Short-chain fatty acids induce intestinal epithelial heat shock protein 25 expression in rats and IEC 18 cells

被引:101
作者
Ren, HY [1 ]
Musch, MW [1 ]
Kojima, K [1 ]
Boone, D [1 ]
Ma, A [1 ]
Chang, EB [1 ]
机构
[1] Univ Chicago, Martin Boyer Res Labs, Chicago, IL 60637 USA
关键词
D O I
10.1053/gast.2001.27028
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims: Because short-chain fatty acids (SCFAs) and heat shock proteins (hsps) confer protection to intestinal epithelia cells (IECs), we studied whether SCFAs modulate IEC hsp expression. Methods: Hsp 25, hsp72, and hsc73 protein expression in rat intestinal tissues and IEC-18 cells were determined by Western blot and immunohistochemistry. Cell survival under conditions of oxidant stress (monochloramine) was determined using Cr-51 release in hsp25 cDNA antisense and sense-transfected cells expressing minimal and increased hsp25, respectively. Results: Butyrate induces a time- and concentration-dependent increase in hsp25, but not hsp72 or hsc73, protein expression in rat IEC-18 cells but not 3T3 fibroblasts. Other SCFAs, including the poorly metabolized isobutyate, also induced selective expression of hsp25. Butyrate treatment significantly improved the ability of IEC-18 cells to withstand oxidant (monochloramine) injury. This effect could be blocked in cells in which hsp25 induction by butyrate was blocked by stable hsp25 antisense transfection. Additionally, hsp25-transfected overexpressing IEC-18 cells showed increased resistance to monochloramine. In vivo, increasing dietary fiber increased colonic, but not proximal, ileal hsp25 while having no effect on hsp72 or hsc73 expression. Conclusions: SCFAs, the predominant anions of colonic fluid derived from bacterial flora metabolism of luminal carbohydrates, protect IECs against oxidant injury, an effect mediated in part by cell-specific hsp25 induction.
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页码:631 / 639
页数:9
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