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10.1186/s12876-017-0627-4

http://scihub22266oqcxt.onion/10.1186/s12876-017-0627-4
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suck abstract from ncbi


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pmid28592228      BMC+Gastroenterol 2017 ; 17 (ä): ä
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  • Anti-fibrogenic effect of PPAR-? agonists in human intestinal myofibroblasts #MMPMID28592228
  • Koo JB; Nam MO; Jung Y; Yoo J; Kim DH; Kim G; Shin SJ; Lee KM; Hahm KB; Kim JW; Hong SP; Lee KJ; Yoo JH
  • BMC Gastroenterol 2017[]; 17 (ä): ä PMID28592228show ga
  • Background: Intestinal fibrosis is a serious complication of inflammatory bowel disease, including Crohn?s disease and ulcerative colitis. There is no specific treatment for intestinal fibrosis. Studies have indicated that peroxisome proliferator-activated receptor- ? (PPAR-?) agonists have anti-fibrogenic properties in organs besides the gut; however, their effects on human intestinal fibrosis are poorly understood. This study investigated the anti-fibrogenic properties and mechanisms of PPAR-? agonists on human primary intestinal myofibroblasts (HIFs). Methods: HIFs were isolated from normal colonic tissue of patients undergoing resection due to colorectal cancer. HIFs were treated with TGF-?1 and co-incubated with or without one of two synthetic PPAR-? agonists, troglitazone or rosiglitazone. mRNA and protein expression of procollagen1A1, fibronectin, and ?-smooth muscle actin were determined by semiquantitative reverse transcription-polymerase chain reaction and Western blot. LY294002 (Akt inhibitor) was used to examine whether Akt phosphorylation was a downstream mechanism of TGF-?1 induced expression of procollagen1A1, fibronectin, and ?-smooth muscle actin in HIFs. The irreversible PPAR-? antagonist GW9662 was used to investigate whether the effect of PPAR-? agonists was PPAR-? dependent. Results: Both PPAR-? agonists reduced the TGF-?1-induced expression of ?-smooth muscle actin which was integrated into stress fibers in HIFs, as determined by actin microfilaments fluorescent staining and ?-smooth muscle actin-specific immunocytochemistry. PPAR-? agonists also inhibited TGF-?1-induced mRNA and protein expressions of procollagen1A1, fibronectin, and ?-smooth muscle actin. TGF-?1 stimulation increased phosphorylation of downstream signaling molecules Smad2, Akt, and ERK. TGF-?1 induced synthesis of procollagen1A1, fibronectin, and ?-smooth muscle actin through a phosphatidylinositol 3-kinase/Akt-dependent mechanism. PPAR-? agonists down regulated fibrogenesis, as shown by inhibition of Akt and Smad2 phosphorylation. This anti-fibrogenic effect was PPAR-? independent. Conclusions: Troglitazone and rosiglitazone suppress TGF-?1-induced synthesis of procollagen1A1, fibronectin, and ?-smooth muscle actin in HIFs and may be useful in treating intestinal fibrosis. Electronic supplementary material: The online version of this article (doi:10.1186/s12876-017-0627-4) contains supplementary material, which is available to authorized users.
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