肿瘤坏死因子α (TNF α)和转化生长因子β 1 (TGF β 1)刺激大鼠肝脏中脂肪储存细胞的纤维连接蛋白合成和向肌成纤维细胞的转分化。

M G Bachem, K M Sell, R Melchior, J Kropf, T Eller, A M Gressner
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引用次数: 122

摘要

转化生长因子- β (TGF - β 1)和肿瘤坏死因子- α (TNF - α)刺激大鼠肝脏中脂肪储存细胞(FSC)向高活性和“合成”的肌成纤维细胞样细胞(MFBIC)的转分化。利用形态学标准(脂肪滴的数量和大小减少,细胞变平和长细胞质延伸的发展),视黄醇棕榈酸酯的损失(通过高效液相色谱测量)和iso- α平滑肌肌动蛋白的表达增强(通过免疫荧光显微镜显示),证明了这种激活。此外,虽然TGF β 1对细胞计数和DNA含量测量的细胞生长有轻微的抑制作用(为对照组的0.81),但TGF β 1与TNF α联合作用对细胞增殖的刺激作用是对照组的1.44倍。此外,TGF β与TNF α联合作用增强了对纤维连接蛋白合成的刺激作用(单独TGF β:对照的1.4倍;单独TNF α:对照组的2.2倍;TGF β + TNF α:对照的4.7倍)。总蛋白合成不受TGF β或TNF α的影响。综上所述,所获得的结果确定TGF β和TNF α是刺激肝纤维化关键事件(即FSC增殖、FSC转分化为MFBIC和纤维连接蛋白合成)的介质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Tumor necrosis factor alpha (TNF alpha) and transforming growth factor beta 1 (TGF beta 1) stimulate fibronectin synthesis and the transdifferentiation of fat-storing cells in the rat liver into myofibroblasts.

Transforming growth factor-beta (TGF beta 1) and tumor necrosis factor alpha (TNF alpha) stimulate the transdifferentiation of fat-storing cells (FSC) in the rat liver into highly active and "synthetic" myofibroblast-like cells (MFBIC). This activation has been documented by differential-interference contrast and light microscopy using morphologic criteria (a reduction in the number and size of fat droplets, cell flattening and the development of long cytoplasmic extensions), by the loss of retinyl-palmitate (measured by HPLC) and by the enhanced expression of iso-alpha smooth muscle actin (demonstrated by immunofluorescence microscopy). Furthermore, while cell growth measured by the cell count and DNA content is slightly inhibited by TGF beta 1 (0.81 of the control), the combination of TGF beta 1 with TNF alpha stimulates cell proliferation to 1.44 times of the control. In addition the combination of TGF beta and TNF alpha potentiated the stimulatory effect on fibronectin synthesis (TGF beta alone: 1.4 times control; TNF alpha alone: 2.2 times control; TGF beta plus TNF alpha: 4.7 times control). The total protein synthesis was not altered by TGF beta or TNF alpha. In summary the results obtained identify TGF beta and TNF alpha as mediators stimulating key events in liver fibrogenesis (i.e. FSC proliferation, FSC transdifferentiation into MFBIC, and fibronectin synthesis).

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