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| ???org.dspace.app.webui.jsptag.ItemTag.dcfield??? | Value | Language |
|---|---|---|
| dc.contributor.advisor | 閔明源(Ming-Yuan Min) | |
| dc.contributor.author | Hock-Ling Chieng | en |
| dc.contributor.author | 錢學霖 | zh_TW |
| dc.date.accessioned | 2021-06-14T17:04:01Z | - |
| dc.date.available | 2010-07-30 | |
| dc.date.copyright | 2008-07-30 | |
| dc.date.issued | 2008 | |
| dc.date.submitted | 2008-07-29 | |
| dc.identifier.citation | References
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Physiol Rev. 83, 117-61. Perrino, C., et al., 2006. Intermittent pressure overload triggers hypertrophy-independent cardiac dysfunction and vascular rarefaction. J Clin Invest. 116, 1547-60. Piedras-Renteria, E. S., et al., 1997. Antisense oligonucleotides against rat brain alpha1E DNA and its atrial homologue decrease T-type calcium current in atrial myocytes. Proc Natl Acad Sci U S A. 94, 14936-41. Porcello, D. M., et al., 2003. Actions of U-92032, a T-type Ca2+ channel antagonist, support a functional linkage between I(T) and slow intrathalamic rhythms. J Neurophysiol. 89, 177-85. Schaible, T. F., Scheuer, J., 1979. Effects of physical training by running or swimming on ventricular performance of rat hearts. J Appl Physiol. 46, 854-60. Scheinowitz, M., et al., 2003. Short- and long-term swimming exercise training increases myocardial insulin-like growth factor-I gene expression. Growth Horm IGF Res. 13, 19-25. Spirito, P., et al., 1994. Morphology of the 'athlete's heart' assessed by echocardiography in 947 elite athletes representing 27 sports. Am J Cardiol. 74, 802-6. Weber, K. T., 1997. Extracellular matrix remodeling in heart failure: a role for de novo angiotensin II generation. Circulation. 96, 4065-82. Wibom, R., et al., 1992. Adaptation of mitochondrial ATP production in human skeletal muscle to endurance training and detraining. J Appl Physiol. 73, 2004-10. Xu, X., Best, P. M., 1992. Postnatal changes in T-type calcium current density in rat atrial myocytes. J Physiol. 454, 657-72. Yeh, J. K., et al., 1994. Effect of growth hormone administration and treadmill exercise on serum and skeletal IGF-I in rats. Am J Physiol. 266, E129-35. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/40863 | - |
| dc.description.abstract | T-型鈣離子通道(T-通道)只短暫表現在胚胎及幼體時期(Leuranguer et al., 2000; Niwa et al., 2004),並跟生長速率有緊密的關係(Xu and Best, 1992)。生長激素(Growth hormone)已知可透過IGF-1(Insulin-like growth hormone)的作用影響動物的體重和心臟的生長(Boguszewski et al., 1997; Ong et al., 2002; Xu and Best, 1991)。另外,IGF-1已被證實可以提高T-通道的電流強度(Piedras-Renteria et al., 1997)。目前發現在運動家生理性肥大心臟中有較多的IGF-1,故推測T-通道可能參與生理性心臟肥大的生成。為探討T-通道在運動引起的心臟肥大所扮演的角色,我們將野生型和CaV3.2型T-通道剔除的老鼠進行長達三週的游泳訓練,同時利用超音波觀察老鼠心臟的變化。在游泳前,野生型和CaV3.2-/-的左心室重量沒有明顯的差異。游泳三週後發現野生型老鼠的左心室明顯變重(0.11 ± 0.0028 (non-swim, n=7) 和0.13 ± 0.0029 (swim, n=7, p<0.001)。但是在CaV3.2-/-的左心室並沒有看到相同的變化(0.1099 ± 0.005 (non-swim, n=5) 和0.1036 ± 0.0028 (swim, n=5), p=0.3)。這個結果指出T-通道在生理性心臟肥大的形成是不可或缺的。 | zh_TW |
| dc.description.abstract | Voltage-gated T-type Ca2+ current (T-current) is temporarily recorded in cardiac myocytes during embryonic and postnatal period in some rodents (Leuranguer et al., 2000; Niwa et al., 2004) and was found linearly correlated with growth rate in rat of both sexes (Xu and Best, 1992). The growth of body weight and heart size has been well studied to be affected by chronically elevated growth hormone (GH) through the action of Insulin-like growth factor-1 (IGF-1) (Boguszewski et al., 1997; Ong et al., 2002; Xu and Best, 1991). Moreover, through the approach of patch-clamp, IGF-1 was found to be able to increase the current density of T-channels (Piedras-Renteria et al., 1997). Collectively, physiological cardiac hypertrophy in athletes is associated with increased cardiac IGF-1 formation, implying that T-channel might play a role in the physiological cardiac hypertrophy formation. To test the hypothesis that T-channels are involved in that cardiac remodeling during physiological cardiac hypertrophy, CaV3.2 T-type calcium channel deficient mice (CaV3.2-/-) were subjected to swimming training for 3 weeks and the development of cardiac hypertrophy was examined with echocardiography. At the basal level, there is no significant difference between wild type (WT) and CaV3.2-/- left ventricular mass (LVM) but after 3 weeks of swimming, WT showed a significant increase of LVM (0.11 ±0.0028 g (WT non-swim, n=7) and 0.13 ± 0.0029 g (WT swim, n=7, p<0.001). In contrast, swimming-induced physiological cardiac hypertrophy was blunted in CaV3.2-/-, the LVM were 0.1099 ± 0.005 (CaV3.2-/- non-swim, n=5) and 0.1036 ± 0.0028 (CaV3.2-/- swim 21ds, n=5, p=0.3). These findings suggest that CaV3.2 is necessary for triggering swimming-induced physiological cardiac hypertrophy. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-14T17:04:01Z (GMT). No. of bitstreams: 1 ntu-97-R95b41010-1.pdf: 699545 bytes, checksum: 9141c5f60ca4e12aa547a1d8647acdde (MD5) Previous issue date: 2008 | en |
| dc.description.tableofcontents | TABLE OF CONTENTS
Page No. Acknowledgements................................I Abstract........................................III Table of Contents...............................VI List of Figures.................................VIII Chapter 1: Introduction 1.1 T-type calcium channel..............1 1.2 Cardiac hypertrophy.................3 1.3 Aim of study........................10 Chapter 2: Materials and Methods 2.1 Animals.............................11 2.2 Swimming exercise protocol..........11 2.3 Pregnancy animal setup..............12 2.4 Echocardiography measurement........12 2.5 Histology...........................13 2.6 Citrate synthase activity assay.....14 2.7 Western analysis....................15 2.8 Neonatal cardiomyocyte isolation and IGF-1 treatment.................17 2.9 Immunofluorescence..................20 2.10 RNA isolation ..................... 21 2.11 Quantitative PCR...................22 2.12 Mouse Insulin-like growth factor I (IGF-1) Immunoassay................23 Chapter 3: Results 3.1 Exercise performance of wild type (WT) and CaV3.2-/- (KO) mice........25 3.2 Responses of WT and KO mice heart to swimming exercise training.......27 3.3 Echocardiography analysis of heart structure in physiological induced cardiac hypertrophy.................28 3.4 IGF-1/PI3K/Akt signaling pathway in swimming mice....................29 3.5 IGF-1 response in neonatal cardiomyocytes......................31 3.6 IGF-1 levels decrease in both WT and KO mice after swimming exercise.32 Chapter 4 : Discussion...........................34 References.......................................38 Figures..........................................41 LIST OF FIGURES Figure 1 Hypertrophic responses following different stimulus......................41 Figure 2 Distinct signaling pathways induced by physiological and pathological hypertrophy.............................42 Figure 3 Evolutionary tree of voltage gated Ca2+ channels...........................43 Figure 4 Swimming apparatus for establishing exercise-induced physiological cardiac hypertrophy.....................44 Figure 5 Swimming-exercise performance in wild type (WT) and CaV3.2-/- (KO) mice..45 Figure 6 Morphometric data from control and swimming WT and CaV3.2-/- (KO) mice.....47 Figure 7 Differential responses of swimming-induced cardiac hypertrophy in WT and CaV3.2-/- (KO) mice...........48 Figure 8 Physiological cardiac hypertrophy responses in late pregnancy WT and CaV3.2-/- (KO) mice.................50 Figure 9 IGF-1/PI3K/AKT signaling protein expression pattern of swimming WT and CaV3.2-/- (KO) mice.................51 Figure 10 IGF-1 levels in non-swim control and 21days swimming trained WT and CaV3.2-/- (KO) mice.....................52 Figure 11 Induction of hypertrophic response of primary cardiomyocytes by IGF-1 and Isoproterenol.......................53 | |
| dc.language.iso | en | |
| dc.title | Cav3.2 T型鈣離子通道參與調控生理性心臟肥大 | zh_TW |
| dc.title | Cav3.2 T-type Calcium Channel Participates in Swimming-induced Physiological Cardiac Hypertrophy | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 96-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.coadvisor | 陳建璋(Chien-Chang Chen) | |
| dc.contributor.oralexamcommittee | 朱柏如(Po-Ju Chu),林恆(Heng Lin) | |
| dc.subject.keyword | 運動,游泳,心臟肥大,T型鈣離子通道,Cav3.2, | zh_TW |
| dc.subject.keyword | t-type calcium channel,cardiac hypertrophy,exercise,swimming, | en |
| dc.relation.page | 54 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2008-07-29 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 動物學研究所 | zh_TW |
| Appears in Collections: | 動物學研究所 | |
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