作者: Hiroshi Kitamura , Shuji Yamamoto , Hiroshi Nakase , Minoru Matsuura , Yusuke Honzawa
DOI: 10.1016/J.BBRC.2010.12.006
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摘要: Abstract Background and aims Intestinal fibrosis is a clinically important issue of inflammatory bowel disease (IBD). It unclear whether or not heat shock protein 47 (HSP47), collagen-specific molecular chaperone, plays critical role in intestinal fibrosis. The aim this study to investigate the HSP47 murine colitis. Methods expression localization were evaluated interleukin-10 knockout (IL-10KO) wild-type (WT, C57BL/6) mice by immunohistochemistry. Expression transforming growth factor-β1 (TGF-β1) colonic tissue was measured. In vitro studies conducted NIH/3T3 cells primary culture myofibroblasts separated from IL-10KO (PMF KO) WT WT) with stimulation several cytokines. We inhibitory effect administration small interfering RNA (siRNA) targeting on vivo. Results Immunohistochemistry revealed positive observed mesenchymal submucosal area both IL-10 KO mice. Gene expressions TGF-β1 significantly higher than correlated severity inflammation. experiments NIH3T3 cells, only induced gene expression. There significant difference between PMF WT. Administration siRNA remarkably reduced collagen deposition Conclusions Our results indicate that an essential mice, may be potential target for associated IBD.