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- W2146795992 abstract "Increased contractility is an important feature of the remodeled airway smooth muscle (ASM) bundle in asthma. The regulation of contractile phenotype marker expression by TGF-β signaling constitutes a key mechanism; however, the underlying molecular mechanisms are poorly understood. Non-canonical WNT signaling is a major regulator of cytoskeletal remodeling and regulates cell movements and polarity during development. Here, we investigated the role of non-canonical WNT signaling in contractile phenotype expression in ASM cells. We used cultured primary and immortalized human ASM cells. Gene expression was analyzed by PCR whereas western blotting and immunocytochemistry were employed for protein expression studies. Serum deprivation or TGF-β treatment induced a contractile ASM phenotype accompanied by an increase in α-sm-actin and calponin. Interestingly, contractile myocytes were markedly enriched in WNT-5A and -11. Knock-down of WNT-5A or -11 using specific siRNA attenuated the TGF-β-induced increase in α-sm-actin protein abundance by 44% and 51%, respectively. Notably, recombinant WNT-5A and -11 were not sufficient to induce contractile phenotype expression in the absence of TGF-β. Further, whereas Smad3 signaling inhibitor (SIS3; 3 μM) reduced TGF-β induced α-sm-actin protein abundance, it did not attenuate WNT-5A and -11 expression, suggesting the cooperative regulation by Smad and WNT-5A/-11 signaling. In conclusion, our data suggest a novel role of WNT-5A and -11 in the regulation of contractile phenotype expression in ASM and provide insight into the mechanisms of airway remodeling." @default.
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- W2146795992 date "2013-09-01" @default.
- W2146795992 modified "2023-09-26" @default.
- W2146795992 title "WNT-5A and WNT-11 as novel regulators of the contractile airway smooth muscle phenotype" @default.
- W2146795992 hasPublicationYear "2013" @default.
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