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对Rho激酶的抑制可通过改变细胞骨架及结缔组织生长因子的表达,调节小肠平滑肌细胞的辐射诱发纤维化显型

世界核心医学期刊文摘（胃肠病学分册） 2005年第7期1卷 31-31页

作者： Bourgier C. haydont v. Milliat F. M.- C.v.zenin- Brotons 陈云茹 Laboratoire UPRES EA 2710 Radiosensibilite Tumeurs/Tissus S. 39 Rue Camille Desmoulins 94805 Villejuif Cedex France Dr.

Background: Late radiation enteritis in humans is associated with accumulatio n of extracellular matrix and increased connectiv. tissue growth factor (CTGF) e xpression that may inv.lv. intestinal muscular layers. Aims: We inv.stigated the molecular pathways inv.lv.d in maintenance of radiation induced fibrosis by gen e profiling and postulated that alteration of the Rho pathway could be associate d with radiation induced fibrogenic signals and CTGF sustained expression. Patie nts and methods: Ileal biopsies from indiv.duals with and without radiation ente ritis were analysed by cDNA array, and primary cultures of intestinal smooth mus cle cells were established. Then, the effect of pharmacological inhibition of p1 60 Rho kinase, using Y- 27632, was studied by real time rev.rse transcription- polymerase chain reaction, western blot, and electrophoretic mobility shift ass ay. Results: Molecular profile analysis of late radiation enteritis showed alter ations in expression of genes coding for the Rho proteins. To inv.stigate furthe r the inv.lv.ment of the Rho pathway in intestinal radiation induced fibrosis, p rimary intestinal smooth muscle cells were isolated from radiation enteritis. Th ey retained their fibrogenic differentiation in v.tro, exhibited a typical cytos keletal network, a high constitutiv. CTGF lev.l, increased collagen secretory ca pacity, and altered expression of genes coding for the Rho family. Rho kinase bl ockade induced a simultaneous decrease in the number of actin stress fibres, α smooth muscle actin, and heat shock protein 27 lev.ls. It also decreased CTGF l ev.ls, probably through nuclear factor κ B inhibition, and caused decreased exp ression of the type I collagen gene. Conclusion: This study is the first showing inv.lv.ment of the Rho/Rho kinase pathway in radiation fibrosis and intestinal smooth muscle cell fibrogenic differentiation. It suggests that specific inhibit ion of Rho kinase may be a promising approach for the dev.lopment of

关键词：肠平滑肌细胞 Rho激酶生长因子细胞骨架放射性小肠炎显型原代培养细胞外基质抑制作用 Ⅰ型胶原基因

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Maintenance of radiation-induced intestinal fibrosis:Cellular and molecular features

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World Journal of Gastroenterology 2007年第19期13卷 2675-2683页

作者： v.lérie haydont Marie-Catherine v.zenin-Brotons UPRES EA 27-10 "Radiosensibilité des tumeurs et tissus sains" Institut de Radioprotection et de Sreté Nucléaire/Institut Gustave Roussy. Villejuif Laboratoire de Radiopathologie. SRBE/DRPH. Institut de Radioprotection et de Sreté Nucléaire Fontenay-aux-Roses France

Recent adv.nces in cell and molecular radiobiology clearly showed that tissue response to radiation injury cannot be restricted to a simple cell-killing process, but depends upon continuous and integrated pathogenic processes, inv.lv.ng cell differentiation and crosstalk between the v.rious cellular components of the tissue within the extracellular matrix. Thus, the prior concept of primary cell target in which a single-cell type （whatev.r it＇s epithelial or endothelial cells） dictates the whole tissue response to radiation injury has to be replaced by the occurrence of coordinated multicellular response that may either lead to tissue recov.ry or to sequel dev.lopment. In this context, the present rev.ew will focus on the maintenance of the radiation-induced wound healing and fibrogenic signals triggered by and through the microenv.ronment toward the mesenchymal cell compartment, and will highlight how sequential and sustained modifications in cell phenotypes will in cascade modify ceU-to-ceU interactions and tissue composition.

关键词： Radiotherapy Fibrosis Fibrogenic differentiation TGF-131 CCN2 Smad Rho ROCK Actincytoskeleton

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