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標題: | 低能量光線對毛囊上皮-間質交互作用的影響:理論與機轉 The effect of low level light on hair follicle epithelial-mesenchymal interaction: theory and mechanism |
作者: | Yi-Shuan Sheen 沈宜萱 |
指導教授: | 紀秀華(Shiou-Hwa Jee) |
關鍵字: | 低能量光線,真皮乳突細胞,生髮,毛囊上皮-間質交互作用, Low level light,dermal papilla cells,hair growth,follicle epithelial-mesenchymal interaction, |
出版年 : | 2009 |
學位: | 碩士 |
摘要: | 毛囊的構造、發育及生長相當複雜,需要密切的上皮-間質交互作用(epithelial-mesenchymal interaction)。來自表皮及真皮的不同訊號,在適當的時間出現,進而造成表皮及真皮的交互作用。而在毛囊發育、生長、週期及病理變化中,毛囊的間質細胞,即真皮乳突細胞(dermal papilla cells),扮演有重要的角色。例如在胚胎發育中,真皮部位形成真皮乳突,乳突細胞與表皮的複雜作用中,逐漸誘導表皮向真皮生長並分化成毛囊。而病態變化中,例如圓形禿(alopecia areata)及雄性禿(androgenetic alopecia) ,許多研究也顯示,真皮乳突細胞的功能受到影響,進而造成掉髮。
低能量的可見光或近紅外光的治療,或稱為低能量光線治療(low level light therapy),近年來已在研究及臨床應用上變成一個相當重要的議題。低能量光線在臨床已有重要的治療應用,其機轉有別於破壞性的高能量雷射,主要是靠直接生物調控(biomodulation)的方式。研究顯示,低能量光線治療可以促進傷口癒合、促進皮膚黑色素細胞再生、保護甲醇引起之視神經傷害、減低大腦之神經傷害、以及促進骨頭修復等。人體細胞如何透過光受體去感受環境的光訊號,進而達到特定的生物效應,這方面的研究正在起步中。 近來,美國食品藥物管理局也核准低能量光線(LaserComb)作為促進頭髮生長之用,但作用機轉並不很清楚。我們假說,低能量光線可能是透過調控真皮乳突細胞,進而調控上皮-間質交互作用,來達到生髮的效果。我們以波長625-635nm發光二極體(light emitting diode)為光源,對真皮乳突細胞照射,結果顯示此光線可以促進真皮乳突細胞的生長,使更多細胞進入分裂期。我們也研究低能量光線促進真皮乳突細胞生長的分子機轉,發現此光線可以使真皮乳突細胞的ERK和Akt磷酸化增加,並且ERK和Akt的抑制劑可以抑制此光線促進細胞增生的效果,顯示此光線可能是藉由活化ERK和Akt來促進真皮乳突細胞的生長。我們同時建立共同培養模型,探討低能量光線對毛囊上皮和間質細胞交互作用的影響。我們發現照射後的真皮乳突細胞,可以分泌因子,促進毛囊上皮細胞的增生。我們認為低能量光線可以活化真皮乳突細胞,並透過毛囊上皮-間質交互作用,來刺激毛囊表皮細胞生長。 The structure, development and growth of hair follicles are very complex and depend on intimate epithelial-mesenchymal interaction. The signals from both the epidermis and dermis contribute to the epidermal and dermal interaction. In follicular development, hair growth, hair cycle, and pathological conditions, the mesenchymal cells of hair follicle, namely dermal papilla cells (DPC), play a vital role. For example in the embryonic stage, the dermal cells condensate into dermal papilla (DP) and epidermal cells bud downward to the dermis and further differentiate into follicular structures under the guidance of DP. In pathological conditions, such as alopecia areata and androgenetic alopecia, a huge body of evidence also suggests the function of DPC is compromised and leads to hair loss. The low level light (LLL) therapy has gained much popularity both in lab researches and clinical applications in recent years. Different from the destructive high energy laser, LLL therapy exerts its effect through direct biomodulation. It has been shown that the LLL therapy is able to promote wound healing, enhance melanocyte regeneration, prevent nerve injury, and facilitate bone repair. The mechanism of the biological effects of LLL therapy has not been investigated in detail. Recently, FDA approved the use of LLL (LaserComb) in hair loss treatment, but the underlying mechanism is unknown. Our hypothesis is that LLL may reach the effect of hair growth via the interaction with DPC to modulate follicle epithelial-mesenchymal interaction. We irradiated DPC with 625-635nm light emitting diode (LED). In comparison with the untreated group, irradiated DPC have a distinct higher rate of proliferation and enhanced cell viability. Also, the treated group has a significant higher proportion of cells in the S/G2M phases of the cell cycle. The levels of ERK and Akt phosphorylation increased significantly 15 minutes post-irradiation. The addition of either PD98059 or LY294002 reversed the growth increase induced by LLL, which showed that LLL affects the growth of DPC quite specifically through both the ERK and the Akt signaling pathways. The number of outer root sheath keratinocytes (ORSK) co-cultured with irradiated DPC was significantly higher than that of the direct-irradiated and control group. The increased proliferation of ORSK in the co-culture system would be explained by indirect action through increased DPC activation in turn mediating ORSK proliferation. We suggest that LLL irradiation simulates the growth of DPC. Furthermore, DPC may increase ORSK proliferation via secreting soluble factors and then modulate hair follicle epithelial-mesenchymal interaction. |
URI: | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/43029 |
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顯示於系所單位: | 臨床醫學研究所 |
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