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首页> 外文期刊>Cell biology international. >Focal adhesion kinase (FAK) siRNA inhibits human hypertrophic scar by suppressing integrin α, TGF-β and α-SMA
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Focal adhesion kinase (FAK) siRNA inhibits human hypertrophic scar by suppressing integrin α, TGF-β and α-SMA

机译：粘着斑激酶（FAK）siRNA通过抑制整合素α，TGF-β和α-SMA抑制人肥厚性瘢痕

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摘要

The effect of focal adhesion kinase (FAK) on suppressing scarring and the potential molecular mechanism underlying it has been investigated. Ten samples of human hypertrophic scars (HS) tissue cultured in vitro were transfected with FAK siRNA mediated by liposome. Quantitative real-time PCR was used to detect the expression of integrin α, transforming growth factor-β (TGF-β), FAK and α-smooth muscle actin (α-SMA) after transfection. MTT assay was used as a measure of fibroblast proliferation. Flow cytometry and 3H-proincorporation technique gave measurements of the cell cycle and the quantity of collagen synthesis, respectively. Expression of FAK was effectively blocked, accompanied by decreasing expression of integrin α, TGF-β and α-SMA in hypertrophic scars fibroblast (HSFB) cells. One to 4 h after transfection with FAK siRNA, proliferation of HSFB cells was strongly inhibited (P0.01), reaching a maximum at 48 h. The proportion of G1 cells was higher and the proportion of the S and G2 cells lower after transfection. The amount of collagen synthesis in HSFB cells decreased when HSFB cells were transfected for 48 h. RNA interference targeting the FAK gene can block the two abnormal signal transduction pathways mediated by the integrin and TGF-β receptors that are responsible for hyperplasia and contracture of the scar, making FAK iRNA therapy a potentially effective approach in HS treatment.
机译：已经研究了粘着斑激酶（FAK）抑制瘢痕形成的作用及其潜在的分子机制。用脂质体介导的FAK siRNA转染十份体外培养的人类肥厚性瘢痕（HS）组织样品。转染后，采用实时荧光定量PCR检测整联蛋白α，转化生长因子-β（TGF-β），FAK和α-平滑肌肌动蛋白（α-SMA）的表达。使用MTT测定法作为成纤维细胞增殖的量度。流式细胞仪和3H原纤维蛋白掺入技术分别测量细胞周期和胶原合成量。 FAK的表达被有效地阻止，伴随着增生性瘢痕成纤维细胞（HSFB）细胞中整联蛋白α，TGF-β和α-SMA的表达降低。用FAK siRNA转染1至4小时后，HSFB细胞的增殖受到强烈抑制（P <0.01），在48小时达到最大值。转染后，G1细胞的比例较高，而S和G2细胞的比例较低。 HSFB细胞转染48 h后，HSFB细胞中胶原蛋白的合成量减少。靶向FAK基因的RNA干扰可以阻断​​由整合素和TGF-β受体介导的两个异常信号转导途径，这两个信号负责疤痕的增生和挛缩，使FAK iRNA疗法成为HS治疗中潜在的有效方法。

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