(<特集>肝臓領域)
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概要
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In response to liver injury, hepatic stellate cell(HSC)dramatically change their phenotype from contractile"quiescent"to synthetic "activated"one, which is a key event in the initiation of fibrogenesis in liver.This so-called myofibroblastic conversion of HSC has been believed to be modulated exclusively by cytokines released by neighboring cells and infiltrated mononuclear cells.Of cytokines implicated in the myofibroblastic conversion, TGF-β can be considered the strongest inducer of the myofibroblastic phenotype.Importantly, recent studies indicate that the TGF-β effect, at least in part, is attributed to stimulation of the sinusoidal endothelial expression of fibronectin containing one of the alternatively spliced segments, ED-A.Moreover, proteolytic fragments of fibronectin, derived from Hep 2 domain, is capable of suppressing the myofibroblastic conversion of HSC by weakening the interaction of HSC with ED-A(+)fibronectin.These results indicate that fibronectin has the potential to serve not only as an up-regulator but also as a down-regulator in the myofibroblastic conversion of HSC.
- 日本結合組織学会の論文
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