【摘要】 目的 原肌球蛋白是肌球蛋白主要相關(guān)蛋白之一，在細(xì)胞骨架與運(yùn)動(dòng)中起著重要的作用。探討原肌球蛋白在增生性瘢痕中的作用，有助于揭示瘢痕攣縮的產(chǎn)生機(jī)制。 方法 收集2006年3月-2008年7月48例患者不同時(shí)期增生與非增生瘢痕組織標(biāo)本，利用基因芯片篩選出的瘢痕相關(guān)基因——原肌球蛋白基因特異片段，制備成寡核苷酸探針與瘢痕組織切片進(jìn)行原位雜交。同時(shí)，將各標(biāo)本進(jìn)行原代細(xì)胞培養(yǎng)，制備成纖維細(xì)胞爬片，進(jìn)行原位雜交。 結(jié)果 原肌球蛋白基因在3、6個(gè)月的增生性瘢痕中表達(dá)均明顯強(qiáng)于9、12個(gè)月增生性瘢痕及非增生性瘢痕，陽性細(xì)胞比例也高于9、12個(gè)月增生性瘢痕及非增生性瘢痕。 結(jié)論 瘢痕增生攣縮與細(xì)胞骨架運(yùn)動(dòng)的相關(guān)基因存在密切關(guān)系，而原肌球蛋白可能在其中起著重要作用。
【Abstract】 Objective Tropomyosin is one of the proteins of cytoskeleton and cell movement. The aim of this study is to investigate the effect of gene expression of fibroblast tropomyosin on the formation and contraction of hypertrophic scar. Methods According to the results of differently expressed genes, in hypertrophic scar by gene microarray, topomyosin, one of the most important genes, was selected and made into oligonucleotide probe. Twenty-four hypertrophic scars and 24 non-hypertrophic scars and 12 normal skins were used and these scar were taken on 3, 6, 9, and 12 months after burned between March 2006 and July 2008. Frozen section and cultured fibroblasts were made to detect the expression of the gene by in situ hybridization. Results Expression of tropomyosin was defected in scar tissue, but those in the hypertrophic scar on 3 and 6 months after burn were significantly ber than those in the hypertrophic scar on 9 and 12 months after burn and non-hypertrophic scar. Conclusion Overexpression of cytoskeletal relative genes causes the contraction of scar and tropomyosin acts leading and key functions.
引用本文： 李晨陽,馬兵,許雪峰,易紹萱,彭陽,孫榆. 原肌球蛋白在增生性瘢痕中的表達(dá)與作用研究. 華西醫(yī)學(xué), 2010, 25(7): 1206-1208. doi: 復(fù)制
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- 1. van der Veer WM, Bloemen MC, Ulrich MM, et al. Potential cellular and molecular causes of hypertrophic scar formation[J]. Burns, 2009, 35(1): 1529. Comment in: Burns, 2010, 36(2): 292-294;author reply 294.
- 2. 馬兵, 吳軍, 易紹萱, 等. 燒傷后早期增生性瘢痕相關(guān)細(xì)胞骨架基因表達(dá)研究[J]. 中華燒傷雜志, 2002, 18(1): 29-31.
- 3. 劉桂林. 細(xì)胞骨架基因相關(guān)蛋白在創(chuàng)傷愈合與瘢痕攣縮中的表達(dá)和作用[J]. 醫(yī)學(xué)綜述, 2007, 13(8): 563-565.
- 4. Murakami K, Stewart M, Nozawa K, et al. Structural basis for tropomyosin overlap in thin(actin)filaments and the generation of a molecular swivel by troponin-T[J]. Proc Natl Acad Sci USA, 2008, 105(20): 7200-7205.
- 5. 王春玲, 邢新. 肌成纖維細(xì)胞與瘢痕[J]. 中國組織工程研究與臨床康復(fù), 2007, 11(6): 1117-1119.
- 6. Lieleg O, Schmoller KM, Claessens MM, et al. Cytoskeletal polymer networks: viscoelastic properties are determined by the microscopic interaction potential of cross-links[J]. Biophys J, 2009, 96(11): 4725-4732.