請用此 Handle URI 來引用此文件：
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/70102完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 謝清河(Ching-Ho Hsieh),陳佑宗(You-Tzung Chen) | |
| dc.contributor.author | Tien-Jui Tsang | en |
| dc.contributor.author | 臧天睿 | zh_TW |
| dc.date.accessioned | 2021-06-17T03:43:35Z | - |
| dc.date.available | 2021-02-22 | |
| dc.date.copyright | 2018-02-22 | |
| dc.date.issued | 2018 | |
| dc.date.submitted | 2018-02-05 | |
| dc.identifier.citation | Abdelnoor, M., Sandven, I., Limalanathan, S., & Eritsland, J. (2014). Postconditioning in ST-elevation myocardial infarction: a systematic review, critical appraisal, and meta-analysis of randomized clinical trials. Vasc Health Risk Manag, 10, 477-491.
Ainsztein, A. M., Kandels-Lewis, S. E., Mackay, A. M., & Earnshaw, W. C. (1998). INCENP centromere and spindle targeting: identification of essential conserved motifs and involvement of heterochromatin protein HP1. J Cell Biol, 143(7), 1763-1774. Altieri, D. C. (2001). The molecular basis and potential role of survivin in cancer diagnosis and therapy. Trends Mol Med, 7(12), 542-547. Altieri, D. C. (2006). Targeted therapy by disabling crossroad signaling networks: the survivin paradigm. Mol Cancer Ther, 5(3), 478-482. doi:10.1158/1535-7163. Ambrosini, G., Adida, C., & Altieri, D. C. (1997). A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma. Nat Med, 3(8), 917-921. Banks, D. P., Plescia, J., Altieri, D. C., Chen, J., Rosenberg, S. H., Zhang, H., & Ng, S. C. (2000). Survivin does not inhibit caspase-3 activity. Blood, 96(12), 4002-4003. Barile, L., Lionetti, V., Cervio, E., Matteucci, M., Gherghiceanu, M., Popescu, L. M., Vassalli, G. (2014). Extracellular vesicles from human cardiac progenitor cells inhibit cardiomyocyte apoptosis and improve cardiac function after myocardial infarction. Cardiovasc Res, 103(4), 530-541. Bergmann, O., Bhardwaj, R. D., Bernard, S., Zdunek, S., Barnabe-Heider, F., Walsh, S., Frisen, J. (2009). Evidence for cardiomyocyte renewal in humans. Science, 324(5923), 98-102. Bishop, J. D., & Schumacher, J. M. (2002). Phosphorylation of the carboxyl terminus of inner centromere protein (INCENP) by the Aurora B Kinase stimulates Aurora B kinase activity. J Biol Chem, 277(31), 27577-27580. Blankenship, J. W., Varfolomeev, E., Goncharov, T., Fedorova, A. V., Kirkpatrick, D. S., Izrael-Tomasevic, A., Vucic, D. (2009). Ubiquitin binding modulates IAP antagonist-stimulated proteasomal degradation of c-IAP1 and c-IAP2(1). Biochem J, 417(1), 149-160. Botker, H. E., Kharbanda, R., Schmidt, M. R., Bottcher, M., Kaltoft, A. K., Terkelsen, C. J., Nielsen, T. T. (2010). Remote ischaemic conditioning before hospital admission, as a complement to angioplasty, and effect on myocardial salvage in patients with acute myocardial infarction: a randomised trial. Lancet, 375(9716), 727-734. Bourhis, E., Hymowitz, S. G., & Cochran, A. G. (2007). The mitotic regulator survivin binds as a monomer to its functional interactor borealin. J Biol Chem, 282(48), 35018-35023. Buerke, M., Murohara, T., Skurk, C., Nuss, C., Tomaselli, K., & Lefer, A. M. (1995). Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion. Proc Natl Acad Sci U S A, 92(17), 8031-8035. Caldas, H., Honsey, L. E., & Altura, R. A. (2005). Survivin 2alpha: a novel survivin splice variant expressed in human malignancies. Mol Cancer, 4(1), 11. Carmena, M., Ruchaud, S., & Earnshaw, W. C. (2009). Making the Auroras glow: regulation of Aurora A and B kinase function by interacting proteins. Curr Opin Cell Biol, 21(6), 796-805. Carmena, M., Wheelock, M., Funabiki, H., & Earnshaw, W. C. (2012). The chromosomal passenger complex (CPC): from easy rider to the godfather of mitosis. Nat Rev Mol Cell Biol, 13(12), 789-803. Chen, Y., Li, D., Liu, H., Xu, H., Zheng, H., Qian, F., Wang, X. (2011). Notch-1 signaling facilitates survivin expression in human non-small cell lung cancer cells. Cancer Biol Ther, 11(1), 14-21. Cheung, C. H., Huang, C. C., Tsai, F. Y., Lee, J. Y., Cheng, S. M., Chang, Y. C., Chang, J. Y. (2013). Survivin - biology and potential as a therapeutic target in oncology. Onco Targets Ther, 6, 1453-1462. Clem, R. J., & Miller, L. K. (1994). Control of programmed cell death by the baculovirus genes p35 and iap. Mol Cell Biol, 14(8), 5212-5222. Cohen, C., Lohmann, C. M., Cotsonis, G., Lawson, D., & Santoianni, R. (2003). Survivin expression in ovarian carcinoma: correlation with apoptotic markers and prognosis. Mod Pathol, 16(6), 574-583. Colnaghi, R., Connell, C. M., Barrett, R. M., & Wheatley, S. P. (2006). Separating the anti-apoptotic and mitotic roles of survivin. J Biol Chem, 281(44), 33450-33456. Conway, E. M., Pollefeyt, S., Cornelissen, J., DeBaere, I., Steiner-Mosonyi, M., Ong, K., Schuh, A. C. (2000). Three differentially expressed survivin cDNA variants encode proteins with distinct antiapoptotic functions. Blood, 95(4), 1435-1442. Cung, T. T., Morel, O., Cayla, G., Rioufol, G., Garcia-Dorado, D., Angoulvant, D., Ovize, M. (2015). Cyclosporine before PCI in Patients with Acute Myocardial Infarction. N Engl J Med, 373(11), 1021-1031. Dai, J., & Higgins, J. M. (2005). Haspin: a mitotic histone kinase required for metaphase chromosome alignment. Cell Cycle, 4(5), 665-668. Dasgupta, P., Kinkade, R., Joshi, B., Decook, C., Haura, E., & Chellappan, S. (2006). Nicotine inhibits apoptosis induced by chemotherapeutic drugs by up-regulating XIAP and survivin. Proc Natl Acad Sci U S A, 103(16), 6332-6337. de Jong, R., Houtgraaf, J. H., Samiei, S., Boersma, E., & Duckers, H. J. (2014). Intracoronary stem cell infusion after acute myocardial infarction: a meta-analysis and update on clinical trials. Circ Cardiovasc Interv, 7(2), 156-167. Deveraux, Q. L., & Reed, J. C. (1999). IAP family proteins--suppressors of apoptosis. Genes Dev, 13(3), 239-252. Dohi, T., Beltrami, E., Wall, N. R., Plescia, J., & Altieri, D. C. (2004). Mitochondrial survivin inhibits apoptosis and promotes tumorigenesis. J Clin Invest, 114(8), 1117-1127. Dohi, T., Okada, K., Xia, F., Wilford, C. E., Samuel, T., Welsh, K., Altieri, D. C. (2004). An IAP-IAP complex inhibits apoptosis. J Biol Chem, 279(33), 34087-34090. Drenckhahn, J. D., Schwarz, Q. P., Gray, S., Laskowski, A., Kiriazis, H., Ming, Z., Cox, T. C. (2008). Compensatory growth of healthy cardiac cells in the presence of diseased cells restores tissue homeostasis during heart development. Dev Cell, 15(4), 521-533. Duckett, C. S., Nava, V. E., Gedrich, R. W., Clem, R. J., Van Dongen, J. L., Gilfillan, M. C., Thompson, C. B. (1996). A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors. EMBO J, 15(11), 2685-2694. Eckelman, B. P., Salvesen, G. S., & Scott, F. L. (2006). Human inhibitor of apoptosis proteins: why XIAP is the black sheep of the family. EMBO Rep, 7(10), 988-994. Erlinge, D., Gotberg, M., Lang, I., Holzer, M., Noc, M., Clemmensen, P., Olivecrona, G. K. (2014). Rapid endovascular catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction. The CHILL-MI trial: a randomized controlled study of the use of central venous catheter core cooling combined with cold saline as an adjunct to percutaneous coronary intervention for the treatment of acute myocardial infarction. J Am Coll Cardiol, 63(18), 1857-1865. Espinosa, M., Ceballos-Cancino, G., Callaghan, R., Maldonado, V., Patino, N., Ruiz, V., & Melendez-Zajgla, J. (2012). Survivin isoform Delta Ex3 regulates tumor spheroid formation. Cancer Lett, 318(1), 61-67. Fujio, Y., Nguyen, T., Wencker, D., Kitsis, R. N., & Walsh, K. (2000). Akt promotes survival of cardiomyocytes in vitro and protects against ischemia-reperfusion injury in mouse heart. Circulation, 101(6), 660-667. Fukuda, S., & Pelus, L. M. (2006). Survivin, a cancer target with an emerging role in normal adult tissues. Mol Cancer Ther, 5(5), 1087-1098. doi:10.1158/1535-7163.MCT-05-0375 Fulda, S., & Vucic, D. (2012). Targeting IAP proteins for therapeutic intervention in cancer. Nat Rev Drug Discov, 11(2), 109-124. Fuller, B. G., Lampson, M. A., Foley, E. A., Rosasco-Nitcher, S., Le, K. V., Tobelmann, P., Kapoor, T. M. (2008). Midzone activation of aurora B in anaphase produces an intracellular phosphorylation gradient. Nature, 453(7198), 1132-1136. Grines, C. L., Watkins, M. W., Mahmarian, J. J., Iskandrian, A. E., Rade, J. J., Marrott, P., Angiogene, G. T. S. G. (2003). A randomized, double-blind, placebo-controlled trial of Ad5FGF-4 gene therapy and its effect on myocardial perfusion in patients with stable angina. J Am Coll Cardiol, 42(8), 1339-1347. Groner, B., & Weiss, A. (2014). Targeting survivin in cancer: novel drug development approaches. BioDrugs, 28(1), 27-39. Guha, M., Plescia, J., Leav, I., Li, J., Languino, L. R., & Altieri, D. C. (2009). Endogenous tumor suppression mediated by PTEN involves survivin gene silencing. Cancer Res, 69(12), 4954-4958. Guo, C., Deng, Y., Liu, J., & Qian, L. (2015). Cardiomyocyte-specific role of miR-24 in promoting cell survival. J Cell Mol Med, 19(1), 103-112. Gyrd-Hansen, M., Darding, M., Miasari, M., Santoro, M. M., Zender, L., Xue, W., Meier, P. (2008). IAPs contain an evolutionarily conserved ubiquitin-binding domain that regulates NF-kappaB as well as cell survival and oncogenesis. Nat Cell Biol, 10(11), 1309-1317. Harvey, A. J., Soliman, H., Kaiser, W. J., & Miller, L. K. (1997). Anti- and pro-apoptotic activities of baculovirus and Drosophila IAPs in an insect cell line. Cell Death Differ, 4(8), 733-744. Hauf, S., Cole, R. W., LaTerra, S., Zimmer, C., Schnapp, G., Walter, R., Peters, J. M. (2003). The small molecule Hesperadin reveals a role for Aurora B in correcting kinetochore-microtubule attachment and in maintaining the spindle assembly checkpoint. J Cell Biol, 161(2), 281-294. Hausenloy, D. J., Candilio, L., Evans, R., Ariti, C., Jenkins, D. P., Kolvekar, S., Investigators, E. T. (2015). Remote Ischemic Preconditioning and Outcomes of Cardiac Surgery. N Engl J Med, 373(15), 1408-1417. Hauser, H. P., Bardroff, M., Pyrowolakis, G., & Jentsch, S. (1998). A giant ubiquitin-conjugating enzyme related to IAP apoptosis inhibitors. J Cell Biol, 141(6), 1415-1422. Henry, T. D., Grines, C. L., Watkins, M. W., Dib, N., Barbeau, G., Moreadith, R., Engler, R. L. (2007). Effects of Ad5FGF-4 in patients with angina: an analysis of pooled data from the AGENT-3 and AGENT-4 trials. J Am Coll Cardiol, 50(11), 1038-1046. Hirohashi, Y., Torigoe, T., Maeda, A., Nabeta, Y., Kamiguchi, K., Sato, T., Sato, N. (2002). An HLA-A24-restricted cytotoxic T lymphocyte epitope of a tumor-associated protein, survivin. Clin Cancer Res, 8(6), 1731-1739. Hirota, T., Lipp, J. J., Toh, B. H., & Peters, J. M. (2005). Histone H3 serine 10 phosphorylation by Aurora B causes HP1 dissociation from heterochromatin. Nature, 438(7071), 1176-1180. Hoffman, W. H., Biade, S., Zilfou, J. T., Chen, J., & Murphy, M. (2002). Transcriptional repression of the anti-apoptotic survivin gene by wild type p53. J Biol Chem, 277(5), 3247-3257. Honda, R., Korner, R., & Nigg, E. A. (2003). Exploring the functional interactions between Aurora B, INCENP, and survivin in mitosis. Mol Biol Cell, 14(8), 3325-3341. Hsieh, P. C., Segers, V. F., Davis, M. E., MacGillivray, C., Gannon, J., Molkentin, J. D., Lee, R. T. (2007). Evidence from a genetic fate-mapping study that stem cells refresh adult mammalian cardiomyocytes after injury. Nat Med, 13(8), 970-974. Hsu, J. Y., Sun, Z. W., Li, X., Reuben, M., Tatchell, K., Bishop, D. K., Allis, C. D. (2000). Mitotic phosphorylation of histone H3 is governed by Ipl1/aurora kinase and Glc7/PP1 phosphatase in budding yeast and nematodes. Cell, 102(3), 279-291. Huang, W., Mao, Y., Zhan, Y., Huang, J., Wang, X., Luo, P., Huang, C. (2016). Prognostic implications of survivin and lung resistance protein in advanced non-small cell lung cancer treated with platinum-based chemotherapy. Oncol Lett, 11(1), 723-730. Jeyaprakash, A. A., Klein, U. R., Lindner, D., Ebert, J., Nigg, E. A., & Conti, E. (2007). Structure of a survivin-borealin-INCENP core complex reveals how chromosomal passengers travel together. Cell, 131(2), 271-285. Jopling, C., Sleep, E., Raya, M., Marti, M., Raya, A., & Izpisua Belmonte, J. C. (2010). Zebrafish heart regeneration occurs by cardiomyocyte dedifferentiation and proliferation. Nature, 464(7288), 606-609. Kanwar, J. R., Kamalapuram, S. K., & Kanwar, R. K. (2013). Survivin signaling in clinical oncology: a multifaceted dragon. Med Res Rev, 33(4), 765-789. Kaufmann, T., Strasser, A., & Jost, P. J. (2012). Fas death receptor signalling: roles of Bid and XIAP. Cell Death Differ, 19(1), 42-50. Kawakami, H., Tomita, M., Matsuda, T., Ohta, T., Tanaka, Y., Fujii, M., Mori, N. (2005). Transcriptional activation of survivin through the NF-kappaB pathway by human T-cell leukemia virus type I tax. Int J Cancer, 115(6), 967-974. Kawashima, S. A., Tsukahara, T., Langegger, M., Hauf, S., Kitajima, T. S., & Watanabe, Y. (2007). Shugoshin enables tension-generating attachment of kinetochores by loading Aurora to centromeres. Genes Dev, 21(4), 420-435. Kelly, A. E., & Funabiki, H. (2009). Correcting aberrant kinetochore microtubule attachments: an Aurora B-centric view. Curr Opin Cell Biol, 21(1), 51-58. Kelly, A. E., Ghenoiu, C., Xue, J. Z., Zierhut, C., Kimura, H., & Funabiki, H. (2010). Survivin reads phosphorylated histone H3 threonine 3 to activate the mitotic kinase Aurora B. Science, 330(6001), 235-239. Kelly, A. E., Sampath, S. C., Maniar, T. A., Woo, E. M., Chait, B. T., & Funabiki, H. (2007). Chromosomal enrichment and activation of the aurora B pathway are coupled to spatially regulate spindle assembly. Dev Cell, 12(1), 31-43. Khan, S., Jutzy, J. M., Aspe, J. R., McGregor, D. W., Neidigh, J. W., & Wall, N. R. (2011). Survivin is released from cancer cells via exosomes. Apoptosis, 16(1), 1-12. Kikuchi, K., Holdway, J. E., Werdich, A. A., Anderson, R. M., Fang, Y., Egnaczyk, G. F., Poss, K. D. (2010). Primary contribution to zebrafish heart regeneration by gata4(+) cardiomyocytes. Nature, 464(7288), 601-605. Kim, P. J., Plescia, J., Clevers, H., Fearon, E. R., & Altieri, D. C. (2003). Survivin and molecular pathogenesis of colorectal cancer. Lancet, 362(9379), 205-209. Klein, U. R., Nigg, E. A., & Gruneberg, U. (2006). Centromere targeting of the chromosomal passenger complex requires a ternary subcomplex of borealin, survivin, and the N-terminal domain of INCENP. Mol Biol Cell, 17(6), 2547-2558. Kobayashi, K., Hatano, M., Otaki, M., Ogasawara, T., & Tokuhisa, T. (1999). Expression of a murine homologue of the inhibitor of apoptosis protein is related to cell proliferation. Proc Natl Acad Sci U S A, 96(4), 1457-1462. Koitabashi, N., Bedja, D., Zaiman, A. L., Pinto, Y. M., Zhang, M., Gabrielson, K. L., Kass, D. A. (2009). Avoidance of transient cardiomyopathy in cardiomyocyte-targeted tamoxifen-induced MerCreMer gene deletion models. Circ Res, 105(1), 12-15. Lee, C. W., Raskett, C. M., Prudovsky, I., & Altieri, D. C. (2008). Molecular dependence of estrogen receptor-negative breast cancer on a notch-survivin signaling axis. Cancer Res, 68(13), 5273-5281. Lee, S. H., Wolf, P. L., Escudero, R., Deutsch, R., Jamieson, S. W., & Thistlethwaite, P. A. (2000). Early expression of angiogenesis factors in acute myocardial ischemia and infarction. N Engl J Med, 342(9), 626-633. Levkau, B., Schafers, M., Wohlschlaeger, J., von Wnuck Lipinski, K., Keul, P., Hermann, S., Baba, H. A. (2008). Survivin determines cardiac function by controlling total cardiomyocyte number. Circulation, 117(12), 1583-1593. Li, C., Wu, Z., Liu, M., Pazgier, M., & Lu, W. (2008). Chemically synthesized human survivin does not inhibit caspase-3. Protein Sci, 17(9), 1624-1629. Li, F., Ambrosini, G., Chu, E. Y., Plescia, J., Tognin, S., Marchisio, P. C., & Altieri, D. C. (1998). Control of apoptosis and mitotic spindle checkpoint by survivin. Nature, 396(6711), 580-584. Li, Q., Li, B., Wang, X., Leri, A., Jana, K. P., Liu, Y., Anversa, P. (1997). Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy. J Clin Invest, 100(8), 1991-1999. Li, S., Wang, L., Meng, Y., Chang, Y., Xu, J., & Zhang, Q. (2017). Increased levels of LAPTM4B, VEGF and survivin are correlated with tumor progression and poor prognosis in breast cancer patients. Oncotarget, 8(25), 41282-41293. Li, X., He, Y., Xu, Y., Huang, X., Liu, J., Xie, M., & Liu, X. (2016). KLF5 mediates vascular remodeling via HIF-1alpha in hypoxic pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol, 310(4), L299-310. Li, X., Liu, X., Xu, Y., Liu, J., Xie, M., Ni, W., & Chen, S. (2014). KLF5 promotes hypoxia-induced survival and inhibits apoptosis in non-small cell lung cancer cells via HIF-1alpha. Int J Oncol, 45(4), 1507-1514. Losordo, D. W., Vale, P. R., Hendel, R. C., Milliken, C. E., Fortuin, F. D., Cummings, N., Kuntz, R. E. (2002). Phase 1/2 placebo-controlled, double-blind, dose-escalating trial of myocardial vascular endothelial growth factor 2 gene transfer by catheter delivery in patients with chronic myocardial ischemia. Circulation, 105(17), 2012-2018. Luo, J., Deng, Z. L., Luo, X., Tang, N., Song, W. X., Chen, J., He, T. C. (2007). A protocol for rapid generation of recombinant adenoviruses using the AdEasy system. Nat Protoc, 2(5), 1236-1247. Mahotka, C., Wenzel, M., Springer, E., Gabbert, H. E., & Gerharz, C. D. (1999). Survivin-deltaEx3 and survivin-2B: two novel splice variants of the apoptosis inhibitor survivin with different antiapoptotic properties. Cancer Res, 59(24), 6097-6102. Marusawa, H., Matsuzawa, S., Welsh, K., Zou, H., Armstrong, R., Tamm, I., & Reed, J. C. (2003). HBXIP functions as a cofactor of survivin in apoptosis suppression. EMBO J, 22(11), 2729-2740. Matsui, T., Tao, J., del Monte, F., Lee, K. H., Li, L., Picard, M., Rosenzweig, A. (2001). Akt activation preserves cardiac function and prevents injury after transient cardiac ischemia in vivo. Circulation, 104(3), 330-335. Mirza, A., McGuirk, M., Hockenberry, T. N., Wu, Q., Ashar, H., Black, S., Liu, S. (2002). Human survivin is negatively regulated by wild-type p53 and participates in p53-dependent apoptotic pathway. Oncogene, 21(17), 2613-2622. Murnion, M. E., Adams, R. R., Callister, D. M., Allis, C. D., Earnshaw, W. C., & Swedlow, J. R. (2001). Chromatin-associated protein phosphatase 1 regulates aurora-B and histone H3 phosphorylation. J Biol Chem, 276(28), 26656-26665. Nowbar, A. N., Mielewczik, M., Karavassilis, M., Dehbi, H. M., Shun-Shin, M. J., Jones, S., group, D. w. (2014). Discrepancies in autologous bone marrow stem cell trials and enhancement of ejection fraction (DAMASCENE): weighted regression and meta-analysis. BMJ, 348, g2688. O'Connor, D. S., Grossman, D., Plescia, J., Li, F., Zhang, H., Villa, A., Altieri, D. C. (2000). Regulation of apoptosis at cell division by p34cdc2 phosphorylation of survivin. Proc Natl Acad Sci U S A, 97(24), 13103-13107. O'Neal, K. R., & Agah, R. (2007). Conditional targeting: inducible deletion by Cre recombinase. Methods Mol Biol, 366, 309-320. Oberpriller, J. O., & Oberpriller, J. C. (1974). Response of the adult newt ventricle to injury. J Exp Zool, 187(2), 249-253. Ottani, F., Latini, R., Staszewsky, L., La Vecchia, L., Locuratolo, N., Sicuro, M., Investigators, C. (2016). Cyclosporine A in Reperfused Myocardial Infarction: The Multicenter, Controlled, Open-Label CYCLE Trial. J Am Coll Cardiol, 67(4), 365-374. Pasumarthi, K. B., Nakajima, H., Nakajima, H. O., Soonpaa, M. H., & Field, L. J. (2005). Targeted expression of cyclin D2 results in cardiomyocyte DNA synthesis and infarct regression in transgenic mice. Circ Res, 96(1), 110-118. Pavlidou, A., Dalamaga, M., Kroupis, C., Konstantoudakis, G., Belimezi, M., Athanasas, G., & Dimas, K. (2011). Survivin isoforms and clinicopathological characteristics in colorectal adenocarcinomas using real-time qPCR. World J Gastroenterol, 17(12), 1614-1621. Pop, C., & Salvesen, G. S. (2009). Human caspases: activation, specificity, and regulation. J Biol Chem, 284(33), 21777-21781. Porrello, E. R., Mahmoud, A. I., Simpson, E., Hill, J. A., Richardson, J. A., Olson, E. N., & Sadek, H. A. (2011). Transient regenerative potential of the neonatal mouse heart. Science, 331(6020), 1078-1080. Poss, K. D., Wilson, L. G., & Keating, M. T. (2002). Heart regeneration in zebrafish. Science, 298(5601), 2188-2190. Pu, Z., Wang, Q., Xie, H., Wang, G., & Hao, H. (2017). Clinicalpathological and prognostic significance of survivin expression in renal cell carcinoma: a meta-analysis. Oncotarget, 8(12), 19825-19833. Quaini, F., Urbanek, K., Beltrami, A. P., Finato, N., Beltrami, C. A., Nadal-Ginard, B., Anversa, P. (2002). Chimerism of the transplanted heart. N Engl J Med, 346(1), 5-15. Richter, B. W., Mir, S. S., Eiben, L. J., Lewis, J., Reffey, S. B., Frattini, A., Duckett, C. S. (2001). Molecular cloning of ILP-2, a novel member of the inhibitor of apoptosis protein family. Mol Cell Biol, 21(13), 4292-4301. Riedl, S. J., Renatus, M., Schwarzenbacher, R., Zhou, Q., Sun, C., Fesik, S. W., Salvesen, G. S. (2001). Structural basis for the inhibition of caspase-3 by XIAP. Cell, 104(5), 791-800. Rodriguez, J. A., Lens, S. M., Span, S. W., Vader, G., Medema, R. H., Kruyt, F. A., & Giaccone, G. (2006). Subcellular localization and nucleocytoplasmic transport of the chromosomal passenger proteins before nuclear envelope breakdown. Oncogene, 25(35), 4867-4879. Rodriguez, J. A., Span, S. W., Ferreira, C. G., Kruyt, F. A., & Giaccone, G. (2002). CRM1-mediated nuclear export determines the cytoplasmic localization of the antiapoptotic protein survivin. Exp Cell Res, 275(1), 44-53. Rosa, J., Canovas, P., Islam, A., Altieri, D. C., & Doxsey, S. J. (2006). Survivin modulates microtubule dynamics and nucleation throughout the cell cycle. Mol Biol Cell, 17(3), 1483-1493. Rosasco-Nitcher, S. E., Lan, W., Khorasanizadeh, S., & Stukenberg, P. T. (2008). Centromeric Aurora-B activation requires TD-60, microtubules, and substrate priming phosphorylation. Science, 319(5862), 469-472. Ross, A. M., Gibbons, R. J., Stone, G. W., Kloner, R. A., Alexander, R. W., & Investigators, A.-I. (2005). A randomized, double-blinded, placebo-controlled multicenter trial of adenosine as an adjunct to reperfusion in the treatment of acute myocardial infarction (AMISTAD-II). J Am Coll Cardiol, 45(11), 1775-1780. Rothe, M., Pan, M. G., Henzel, W. J., Ayres, T. M., & Goeddel, D. V. (1995). The TNFR2-TRAF signaling complex contains two novel proteins related to baculoviral inhibitor of apoptosis proteins. Cell, 83(7), 1243-1252. Roy, N., Mahadevan, M. S., McLean, M., Shutler, G., Yaraghi, Z., Farahani, R., et al. (1995). The gene for neuronal apoptosis inhibitory protein is partially deleted in individuals with spinal muscular atrophy. Cell, 80(1), 167-178. Ruchaud, S., Carmena, M., & Earnshaw, W. C. (2007). Chromosomal passengers: conducting cell division. Nat Rev Mol Cell Biol, 8(10), 798-812. Ryan, B., O'Donovan, N., Browne, B., O'Shea, C., Crown, J., Hill, A. D., Duffy, M. J. (2005). Expression of survivin and its splice variants survivin-2B and survivin-DeltaEx3 in breast cancer. Br J Cancer, 92(1), 120-124. Ryan, B. M., O'Donovan, N., & Duffy, M. J. (2009). Survivin: a new target for anti-cancer therapy. Cancer Treat Rev, 35(7), 553-562. Sabbattini, P., Canzonetta, C., Sjoberg, M., Nikic, S., Georgiou, A., Kemball-Cook, G., Dillon, N. (2007). A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells. EMBO J, 26(22), 4657-4669. Salman, T., Argon, A., Kebat, T., Vardar, E., Erkan, N., & Alacacioglu, A. (2016). The prognostic significance of survivin expression in gallbladder carcinoma. APMIS, 124(8), 633-638. Santini, D., Abbate, A., Scarpa, S., Vasaturo, F., Biondi-Zoccai, G. G., Bussani, R., Baldi, A. (2004). Surviving acute myocardial infarction: survivin expression in viable cardiomyocytes after infarction. J Clin Pathol, 57(12), 1321-1324. Sarkar, N., Ruck, A., Kallner, G., S, Y. H., Blomberg, P., Islam, K. B., Sylven, C. (2001). Effects of intramyocardial injection of phVEGF-A165 as sole therapy in patients with refractory coronary artery disease--12-month follow-up: angiogenic gene therapy. J Intern Med, 250(5), 373-381. Shin, S., Sung, B. J., Cho, Y. S., Kim, H. J., Ha, N. C., Hwang, J. I., Oh, B. H. (2001). An anti-apoptotic protein human survivin is a direct inhibitor of caspase-3 and -7. Biochemistry, 40(4), 1117-1123. Siddiquee, K., Zhang, S., Guida, W. C., Blaskovich, M. A., Greedy, B., Lawrence, H. R., Turkson, J. (2007). Selective chemical probe inhibitor of Stat3, identified through structure-based virtual screening, induces antitumor activity. Proc Natl Acad Sci U S A, 104(18), 7391-7396. Sohal, D. S., Nghiem, M., Crackower, M. A., Witt, S. A., Kimball, T. R., Tymitz, K. M., Molkentin, J. D. (2001). Temporally regulated and tissue-specific gene manipulations in the adult and embryonic heart using a tamoxifen-inducible Cre protein. Circ Res, 89(1), 20-25. Stone, G. W., Martin, J. L., de Boer, M. J., Margheri, M., Bramucci, E., Blankenship, J. C., Investigators, A.-I. T. (2009). Effect of supersaturated oxygen delivery on infarct size after percutaneous coronary intervention in acute myocardial infarction. Circ Cardiovasc Interv, 2(5), 366-375. Suga, K., Yamamoto, T., Yamada, Y., Miyatake, S., Nakagawa, T., & Tanigawa, N. (2005). Correlation between transcriptional expression of survivin isoforms and clinicopathological findings in human colorectal carcinomas. Oncol Rep, 13(5), 891-897. Sun, Y. W., Xuan, Q., Shu, Q. A., Wu, S. S., Chen, H., Xiao, J., Zhao, S. T. (2013). Correlation of tumor relapse and elevated expression of survivin and vascular endothelial growth factor in superficial bladder transitional cell carcinoma. Genet Mol Res, 12(2), 1045-1053. Tamm, I., Wang, Y., Sausville, E., Scudiero, D. A., Vigna, N., Oltersdorf, T., & Reed, J. C. (1998). IAP-family protein survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax, caspases, and anticancer drugs. Cancer Res, 58(23), 5315-5320. Tseng, B. S., Tan, L., Kapoor, T. M., & Funabiki, H. (2010). Dual detection of chromosomes and microtubules by the chromosomal passenger complex drives spindle assembly. Dev Cell, 18(6), 903-912. Uren, A. G., Wong, L., Pakusch, M., Fowler, K. J., Burrows, F. J., Vaux, D. L., & Choo, K. H. (2000). Survivin and the inner centromere protein INCENP show similar cell-cycle localization and gene knockout phenotype. Curr Biol, 10(21), 1319-1328. Vader, G., Kauw, J. J., Medema, R. H., & Lens, S. M. (2006). Survivin mediates targeting of the chromosomal passenger complex to the centromere and midbody. EMBO Rep, 7(1), 85-92. van der Waal, M. S., Hengeveld, R. C., van der Horst, A., & Lens, S. M. (2012). Cell division control by the Chromosomal Passenger Complex. Exp Cell Res, 318(12), 1407-1420. Vucic, D., Stennicke, H. R., Pisabarro, M. T., Salvesen, G. S., & Dixit, V. M. (2000). ML-IAP, a novel inhibitor of apoptosis that is preferentially expressed in human melanomas. Curr Biol, 10(21), 1359-1366. Wang, F., Dai, J., Daum, J. R., Niedzialkowska, E., Banerjee, B., Stukenberg, P. T., Higgins, J. M. (2010). Histone H3 Thr-3 phosphorylation by Haspin positions Aurora B at centromeres in mitosis. Science, 330(6001), 231-235. Wang, H., Holloway, M. P., Ma, L., Cooper, Z. A., Riolo, M., Samkari, A., Altura, R. A. (2010). Acetylation directs survivin nuclear localization to repress STAT3 oncogenic activity. J Biol Chem, 285(46), 36129-36137. Wang, Y. F., Ma, S. R., Wang, W. M., Huang, C. F., Zhao, Z. L., Liu, B., Sun, Z. J. (2014). Inhibition of survivin reduces HIF-1alpha, TGF-beta1 and TFE3 in salivary adenoid cystic carcinoma. PLoS One, 9(12), e114051. White, S. K., Frohlich, G. M., Sado, D. M., Maestrini, V., Fontana, M., Treibel, T. A., Hausenloy, D. J. (2015). Remote ischemic conditioning reduces myocardial infarct size and edema in patients with ST-segment elevation myocardial infarction. JACC Cardiovasc Interv, 8(1 Pt B), 178-188. Wong, R. S. (2011). Apoptosis in cancer: from pathogenesis to treatment. J Exp Clin Cancer Res, 30, 87. Woo, J. S., Kim, W., Ha, S. J., Kim, J. B., Kim, S. J., Kim, W. S., Kim, K. S. (2013). Cardioprotective effects of exenatide in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention: results of exenatide myocardial protection in revascularization study. Arterioscler Thromb Vasc Biol, 33(9), 2252-2260. Xing, Z., Conway, E. M., Kang, C., & Winoto, A. (2004). Essential role of survivin, an inhibitor of apoptosis protein, in T cell development, maturation, and homeostasis. J Exp Med, 199(1), 69-80. Yamada, Y., Kuroiwa, T., Nakagawa, T., Kajimoto, Y., Dohi, T., Azuma, H., Miyatake, S. (2003). Transcriptional expression of survivin and its splice variants in brain tumors in humans. J Neurosurg, 99(4), 738-745. Yamagishi, Y., Honda, T., Tanno, Y., & Watanabe, Y. (2010). Two histone marks establish the inner centromere and chromosome bi-orientation. Science, 330(6001), 239-243. Yang, B., Yan, P., Gong, H., Zuo, L., Shi, Y., Guo, J., Li, B. (2016). TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner. Am J Transl Res, 8(9), 3848-3860. Yu, J. I., Lee, H., Park, H. C., Choi, D. H., Choi, Y. L., Do, I. G., Park, W. (2016). Prognostic significance of survivin in rectal cancer patients treated with surgery and postoperative concurrent chemo-radiation therapy. Oncotarget, 7(38), 62676-62686. Zhang, T., Otevrel, T., Gao, Z., Gao, Z., Ehrlich, S. M., Fields, J. Z., & Boman, B. M. (2001). Evidence that APC regulates survivin expression: a possible mechanism contributing to the stem cell origin of colon cancer. Cancer Res, 61(24), 8664-8667. Zwerts, F., Lupu, F., De Vriese, A., Pollefeyt, S., Moons, L., Altura, R. A., Conway, E. M. (2007). Lack of endothelial cell survivin causes embryonic defects in angiogenesis, cardiogenesis, and neural tube closure. Blood, 109(11), 4742-4752. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/70102 | - |
| dc.description.abstract | 心肌梗塞（心臟病發作）為心血管疾病中最致命的死因之一，而心血管疾病在台灣十大死因中長居第二排名。雖然目前在臨床上已經有血管再灌注手術以及藥物的治療，但是由於成人心臟所具有的復原能力非常微弱，病人在接受治療之後仍然有很高的機率會面臨到慢性心臟衰竭的危害。因此除了傳統的治療方式之外，搭配基因治療具有能夠更有效的解決心肌梗塞病人所可能遭遇到的長期問題之潛力。
Survivin是抑制細胞凋亡家族（inhibitor of apoptosis family）中最小的成員。Survivin除了具有在細胞凋亡過程中能夠抑制凋零蛋白酶-9（caspase-9）活化的能力，也具備在細胞分裂中調控染色體分離的功能。之前的研究發現在心肌細胞專一survivin基因剔除鼠中，缺少survivin會造成心肌細胞不完整的細胞分裂進而影響到心臟的發育。然而，survivin在心肌梗塞之後心肌細胞中的功能仍然不清楚。 在研究中，我們建立了誘發性心肌細胞專一survivin基因剔除鼠。在此基因剔除鼠中我們發現缺血心肌組織周圍有30.8%的心肌細胞進行細胞凋亡，明顯高於在對照組老鼠中只有22.2%的比例。術後21天對照組老鼠具有38.0%的心室輸出容積比例（ejection fraction），而基因剔除鼠卻降至29.0%。當我們在老鼠的心肌細胞細胞質中大量表現survivin，老鼠在心肌梗塞後相較於對照組，會有較高的心室輸出容積比例、較少的心肌細胞凋亡、以及較低比例的凋零蛋白酶-3活化。然而，心肌細胞細胞核內有大量的survivin表現，可以在術後的老鼠發現更多的心肌細胞增殖，而這樣的結果是survivin經由與Aurora B的交互作用造成。 在我們的研究中，我們展示了survivin在心肌細胞中不同的位置會具有不同的功能，而survivin在心肌細胞中所扮演的角色也與心肌梗塞後的回復有著相當重要的關聯。在未來，配合著心肌細胞專一以及較少免疫反應的給予方式，survivin非常具有潛力應用在心肌梗塞的臨床治療。 | zh_TW |
| dc.description.abstract | Myocardial infarction, commonly known as heart attack, is a possibly fatal result of cardiovascular disease, which is the second leading cause of death in Taiwan. Even though catheter-based and surgical revascularization plus pharmacological therapies are available for patients with acute myocardial infarction, a substantial portion of patients develop heart failure, with poor cardiac regeneration. Therefore, for such patients, novel and advanced therapies are needed; among the foreseeable possibilities, gene therapy is a good candidate.
Survivin is the smallest member of the inhibitor of apoptosis family. It has two important functions; inhibition of caspase-9 activation during apoptosis, and regulation of chromosome segregation during cell division. Genetic depletion of cardiac survivin leads to incomplete cardiomyocyte division and abnormal heart development. However, the function of survivin in adult hearts after myocardial infarction remains unclear. We found that 30.8% of cardiomyocytes in the peri-infarct region of inducible cardiomyocyte-specific survivin knockout mice were apoptotic, a significantly higher percentage than 22.2% in control mice. Ejection fraction was 29.0% in knockout mice compared to 38.0% in control mice 21 days after MI. However, mice overexpressing cytosolic survivin maintained a 8.7% higher ejection fraction, had 4.7% fewer apoptotic cardiomyocytes, and showed reduced activation of caspase-3 compared to control mice. Moreover, mice overexpressing survivin contained a nuclear localization sequence and exhibited enhanced cardiomyocyte proliferation through interaction with Aurora B. Here, we demonstrate the importance of survivin subcellular localization in regulating post-MI cardiac repair and regeneration, and show the translational potential of targeted delivery of survivin. Its cardiac-specific regulation of expression coupled with less immune responsive gene delivery, suggests that survivin is a potential future clinical therapeutic candidate in the treatment of myocardial infarction. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T03:43:35Z (GMT). No. of bitstreams: 1 ntu-107-D00421005-1.pdf: 4944662 bytes, checksum: 5107d8fac8ffd291e16f4fe54ed4bbbe (MD5) Previous issue date: 2018 | en |
| dc.description.tableofcontents | 口試委員會鑑定書………………………………………………………………..……..i
誌謝………………………………………………………………………………….…..ii Table of contents………………………………………………………………………...iii 摘要…………………………………………………………………………………....viii Abstract……………………………………………………………………………….…ix Chapter 1. Introduction……………………………………………………………...…1 1.1 Myocardial infarction is a leading cause of morbidity and mortality worldwide…1 1.1.1 Cardiac regeneration ability is limited in adult mammalian heart …......…….3 1.2 Survivin (SVV) is multi-functional in cell apoptosis and proliferation……..……5 1.2.1 Inhibitor of apoptosis protein (IAP) family attenuates cell apoptosis……..…5 1.2.1.1 SVV is the smallest member of the IAP family…………………………...7 1.2.2 Apoptosis is a process of programmed cell death.…………………………..10 1.2.2.1 SVV inhibits cell apoptosis……………………………………………..12 1.2.3 Chromosomal passenger complex (CPC) is essential in mitosis…..………..13 1.2.3.1 SVV modulates microtubule organization and chromosome segregation during cell mitosis………………………………………………………15 1.2.4 Subcellular localization of SVV is not restrained in the nucleus or the cytoplasm…..………………………………………………………………16 1.2.5 SVV is essential in mouse development…………………………………....17 1.3 The Cre-loxP system allows spatial- and temporal-specific gene ablation in mice…………………………………………………………………...……..…19 1.4 Thesis hypothesis and aims……………..………………………………………21 Chapter 2. Materials and Methods……………………………………………..…….22 2.1 Animals…………………………………………………………………………22 2.2 RT-PCR analysis…………………………………………………….………….22 2.3 Western blotting………………………………………………………..……….23 2.4 Immunohistochemical staining…………………………………………………23 2.5 Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining………………………………………………………..……………...…25 2.6 Adenovirus establishment………..……………………………………………..25 2.7 Trichrome staining……………………..…………………………………...…..26 2.8 Animal surgery and echocardiography…………..……………………………..26 2.9 Statistics…………………………..………………………………………….....27 Chapter 3. Results…………………………………………………………………..…28 3.1 Cardiac SVV expression attenuates after birth but is re-activated after MI……...28 3.2 Cardiac specific, inducible SVV knockout mice have lower cardiac recovery ability………………………………………………………………………...…30 3.3 Overexpressing SVV attenuates cardiomyocyte apoptosis………………….….32 3.4 Adenoviral overexpression of SVV improves post-MI cardiac function………..34 3.5 Nuclear SVV enhances cardiomyocyte proliferation……..…………………….35 3.6 Intramyocardial injection of adNLS-SVV promotes cardiomyocyte regeneration………………………………………………………..…………...37 Chapter 4. Discussion…………………………………………………………….……39 4.1 Subcellular localization of endogenous SVV is highly regulated in cardiomyocytes………………………………………………………………....39 4.2 Cytosolic SVV in cardiomyocytes is essential in recovery of cardiac function after MI……………………………………………………………………………….42 4.3 Cytosolic SVV inhibits apoptosis in cardiomyocytes through caspase-9…...…..45 4.4 Nuclear SVV enhances cardiomyocyte proliferation through Aurora B……...…48 4.5 Expression of SVV is activated in cardiomyocytes after MI……...……….….....51 4.6 NLS-SVV exhibits extra cell proliferation enhancement than SVV…………….55 Chapter 5. Perspective……………………………………………………………..….60 5.1 SVV is a potential candidate for cardiac recovery therapy after MI……….…….60 5.2 Exogenous NLS-SVV should be overexpressed specifically in cardiomyocytes.63 5.3 Adeno-associated viral vector is a potential gene delivery system for MI therapy…………………………………………….………..…………………..65 Chapter 6. Summary…………………………………………………………………..70 Chapter 7. References…………………………………………………………………80 Chapter 8. Tables and figures………………………………………………………..102 Table 1. Cardiac function of mice received intramyocardial virus injection and coronary artery ligation……………………………………………...…..102 Figure 1. SVV locates in the nucleus of proliferating cardiomyocyte during heart development…………………………………………………………….103 Figure 2. SVV is upregulated in the cytoplasm of cardiomyocytes after MI………105 Figure 3. Isoforms and regulator of SVV in heart development and after injury…..107 Figure 4. Establishment of inducible cardiac-specific SVV knockout mouse……..108 Figure 5. SVV is successfully knocked out in cardiomyocyte of KO mouse after MI……………………………………………………………………….109 Figure 6. Cardiac functions of KO mouse is worse compared to MCM mouse 21 days after MI………………………………………………………………….110 Figure 7. Apoptotic cardiomyocytes are increased in KO mouse after MI………...111 Figure 8. Proliferating cardiomyocyte in MCM and KO mice after MI……………112 Figure 9. Evaluation of scar formation in MCM and KO mice 30 days post MI…...113 Figure 10. Examination of cardiomyocyte size in MCM and KO mice after MI…....115 Figure 11. Localization of endogenous and exogenous SVV in neonatal mouse cardiomyocytes overexpressing SVV or NLS-SVV…………………….116 Figure 12. Overexpression of SVV attenuates cardiomyocyte apoptosis…………...117 Figure 13. Mutant SVV T34A loses its anti-apoptotic function……………………..119 Figure 14. Mutant SVV-T34A is not able to interact with caspase-9………………..120 Figure 15. Delivery efficiency and localization of treatment using intramyocardial injection of virus………………………………………………………...121 Figure 16. Administration of SVV attenuates cardiomyocyte apoptosis in vivo…….123 Figure 17. Overexpression of SVV recuses cardiac function after infarction……….125 Figure 18. Overexpression of SVV attenuates scar formation after infarction……...126 Figure 19. NLS-SVV enhances cardiomyocyte proliferation through Aurora B……127 Figure 20. NLS-SVV enhances cardiomyocyte proliferation after injury in vivo…...128 Figure 21. Overexpression of NLS-SVV reduces loss of cardiac functions after infarction………………………………………………………………..130 Figure 22. Overexpression of NLS-SVV attenuates scar formation after infarction..131 Figure 23. Schematic diagram of SVV function in cardiomyocyte after MI……...…132 Chapter 9. Appendix……………………………………………………………...….133 Publication……………………………………………………………………….…133 | |
| dc.language.iso | en | |
| dc.title | Survivin在心肌再生中扮演的角色 | zh_TW |
| dc.title | The role of survivin in cardiac regeneration | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 106-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 楊偉勛(Wei-Shiung Yang),江伯倫(Bor-Luen Chiang),葉宏一(Hung-I Yeh),陳建璋(Chein-Chang Chen) | |
| dc.subject.keyword | 心肌再生,基因治療,心肌梗塞,細胞內位置,survivin, | zh_TW |
| dc.subject.keyword | cardiac regeneration,gene therapy,myocardial infarction,subcellular localization,survivin, | en |
| dc.relation.page | 133 | |
| dc.identifier.doi | 10.6342/NTU201800250 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2018-02-05 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 臨床醫學研究所 | zh_TW |
| 顯示於系所單位： | 臨床醫學研究所 | |
文件中的檔案：
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-107-1.pdf 目前未授權公開取用 | 4.83 MB | Adobe PDF |
系統中的文件，除了特別指名其著作權條款之外，均受到著作權保護，並且保留所有的權利。