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題名 | 豬主動脈平滑肌細胞表現型調節之探討=Phenotypic Modulation of Smooth Nuscle Cells from Porcine Aorta |
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作者姓名(中文) | 黃琇琴; 李文權; 陳世平; 楊平政; 毛仁淡; | 書刊名 | 中華民國獸醫學會雜誌 |
卷期 | 23:3 1997.06[民86.06] |
頁次 | 頁293-302 |
分類號 | 437.657 |
關鍵詞 | 表現型調節; 合生期; α平滑肌動蛋白; 平滑肌凝蛋白; Phenotypic modulation; Confluence; α-smooth muscle actin; Smooth muscle myosin; |
語文 | 中文(Chinese) |
中文摘要 | 許多的研究指出,動脈硬化及血管再阻塞的病變過程中,血管平滑肌細胞有表現 型調節的作用。在本實驗中,我們分離培養豬主動脈平滑肌細胞,以α-平滑肌動蛋白 (α -SMA) 及平滑肌凝蛋白 (SMM) 為標誌蛋白, 確定平滑肌細胞之特性,並建立研究表現型調 節的細胞模式。將細胞培養在含 10 %胎牛血清的培養液中,可看出細胞形態依著不同生長 階段而改變;分別為合生前期 (SC)、合生期 (C)、合生後期 (PC)、和鈕釦期 (N)。利用西 方免疫吸漬法,以相同的細胞數目或總蛋白質量為依據, 比較 4 個細胞生長階段α- SMA 及 SMM 的變化,更進一步發現,在 PC 和 N 兩個階段時,α- SMA 及 SMM 的量較 SC 增 加 50-70 %。電子顯微鏡的結果也顯示,SC 時期的細胞質內含較多的粗內質網、高基氏體 和囊泡。 而在 N 期的細胞質內則含有成束的肌纖維。 綜合不同培養階段α- SMA 及 SMM 量及形態學上的變化來看,平滑肌細胞的確發生表現型調節;此可模擬動脈硬化及血管再阻 塞時血管壁中層及新內層之平滑肌細胞之特性。將來可進一步應用此細胞模式研究相關疾病 之預防及治療藥物,以降低動脈硬化及血管再阻塞之發生率。 |
英文摘要 | It has been documented that phenotypic modulation of vascular smooth muscle cells (SMC) is involved in the pathogenesis of atherosclerosis and restenosis. In this study, we report an in vitro model for the investigation of phenotypic modulation of SMC. SMC isolated from porcine aorta were confirmed using marker proteins α -smooth muscle actin (α -SMA) and smooth muscle myosin (SMM). When cultured in medium supplemented with 10% FBS, however, a dramatic change in morphology at four stages subconfluence (SC), confluence (C), postconfluence (PC), and nodule (N) was observed. Using Western immunostaining with loading either equal cell number or protein amount, the level of α -SMA and SMM increased 50-70% in the cells at the latter two stages when compared to the SC cells. Results from electron microscopy showed that the cells at the SC stage contained well-developed rough endoplasmic reticulum and Golgi appratus togethered with numerous vesicles, however, there was few myofilament to be observed. In contrast., myofilaments was increased and well organized at the stage N. The alterations of α -SMA, SMM and morphologic changes described in this study mimic that of phenotypic status of SMC in the media and neointima possible of atherosclerosis and restenosis. Further studies on possible drug intervention of the related disease are currently undertaking using this cellular model. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。