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10.3748/wjg.v23.i13.2330

http://scihub22266oqcxt.onion/10.3748/wjg.v23.i13.2330
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C5385399!5385399!28428712
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suck abstract from ncbi


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pmid28428712      World+J+Gastroenterol 2017 ; 23 (13): 2330-6
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  • Notch signaling mediated by TGF-?/Smad pathway in concanavalin A-induced liver fibrosis in rats #MMPMID28428712
  • Wang Y; Shen RW; Han B; Li Z; Xiong L; Zhang FY; Cong BB; Zhang B
  • World J Gastroenterol 2017[Apr]; 23 (13): 2330-6 PMID28428712show ga
  • AIM: To explore the exact interaction between Notch and transforming growth factor (TGF)-? signaling in liver fibrosis. METHODS: We established a rat model of liver fibrosis induced by concanavalin A. Peripheral blood mononuclear cells (PBMCs) were isolated from the modeled rats, and cultured with ?-secretase inhibitor DAPT and TGF-? inhibitor for 24 h. The mRNA levels of Notch and TGF-? signaling were detected by quantitative real-time polymerase chain reaction. Expression of Notch and TGF-? proteins was analyzed by western blotting. RESULTS: Compared to control rats, Notch and TGF-? signaling was activated in PBMCs of model rats. Administration of DAPT and TGF-? inhibitor suppressed Notch and TGF-? signal transducer in PBMCs of model rats. DAPT reduced mRNA and protein expression of TGF-? signaling, such as TGF-?1 and Smad3. TGF-? inhibitor also downregulated Notch1, Hes1 and Hes5, and mRNA and protein expression of the Notch signaling pathway. CONCLUSION: Notch and TGF-? signaling play a role in liver fibrosis. TGF-? signaling upregulates Notch signaling, which promotes TGF-? signaling.
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