AIM: To investigate the role of canonical transient receptor potential channel 1 (TRPC1) in the epithelial-mesenchymal transition (EMT) of human bronchial epithelial (HBE) cells induced by transforming growth factor-β1 (TGF-β1). METHODS: EMT of 16HBE cells induced by TGF-β1 were identified by microscopy, immunofluorescence and Western blotting. Immunofluorescence, real-time PCR and Western blotting were applied to detect the mRNA and the protein expression of TRPC1 in the 16HBE cells. The influence of SKF96365 (a TRPC1 blocker) and siRNA-mediated silencing of TRPC1 on the EMT of the 16HBE cells were detected by microscopy and Western blotting. RESULTS: Treatment with TGF-β1 induced significant morphological changes of the 16HBE cells. Exposure to TGF-β1 decreased the expression of E-cadherin protein (P<0.01) and increased the expression of α-SMA protein (P<0.05) in the 16HBE cells. Immunofluorescence observation indicated that TRPC1 expression in the 16HBE cells was positive. The expression of TRPC1 at mRNA and protein levels was significantly increased in the 16HBE cells after stimulation with TGF-β1 (P<0.05). The morphological changes of the 16HBE cells induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silencing compared with TGF-β1 group. The protein expression of E-cadherin and α-SMA induced by TGF-β1 were inhibited by SKF96365 and TRPC1 silencing compared with TGF-β1 group (P<0.05). CONCLUSION: TGF-β1 induces EMT with the mechanism of up-regulating TRPC1 in human bronchial epithelial cells.
Homer RJ, Elias JA. Airway remodeling in asthma: therapeutic implications of mechanisms[J]. Physiology (Bethesda), 2005, 20(2):28-35.
[4]
Willis BC, Borok Z. TGF-beta-induced EMT: mechanisms and implications for fibrotic lung disease[J]. Am J Physiol Lung Cell Mol Physiol, 2007,293(3):L525-L534.
[5]
Shen HJ, Sun YH, Zhang SJ, et al. Cigarette smoke-induced alveolar epithelial-mesenchymal transition is mediated by Rac1 activation[J]. Biochim Biophys Acta, 2014, 1840(6):1838-1849.
[6]
Lv ZD, Kong B, Li JG, et al. Transforming growth factor-beta 1 enhances the invasiveness of breast cancer cells by inducing a Smad2-dependent epithelial-to-mesenchymal transition[J]. Oncol Rep, 2013, 29(1):219-225.
[7]
Mahaut-Smith MP. A role for platelet TRPC channels in the Ca2+ response that induces procoagulant activity[J]. Sci Signal, 2013, 6(281):pe23.
[8]
Madsen CP, Klausen TK, Fabian A, et al. On the role of TRPC1 in control of Ca2+ influx, cell volume, and cell cycle[J]. Am J Physiol Cell Physiol, 2012, 303(6):C625-C634.
[9]
Reyes RC, Verkhratsky A, Parpura V. TRPC1-mediated Ca2+ and Na+ signaling in astroglia: differential filtering of extracellular cations[J]. Cell Calcium, 2013, 54(2):120-125.
[10]
Zhang M, Zhang Z, Pan HY, et al. TGF-beta1 induces human bronchial epithelial cell-to-mesenchymal transition in vitro[J]. Lung, 2009, 187(3):187-194.
[11]
Kim JH, Jang YS, Eom KS, et al. Transforming growth factor β1 induces epithelial-to-mesenchymal transition of A549 cells[J]. J Korean Med Sci, 2007, 22(5):898-904.
[12]
Xu J, Lamouille S, Derynck R. TGF-β-induced epithelial to mesenchymal transition[J]. Cell Res, 2009, 19(2):156-172.