Significance Of TGF-β1 In Rat Alveolar Epithelial Cells With CSE-Induced Cell Cycle Transformation

Objective:To describe the effect of TGF-β1 on cell cycle alteration induced by cigarette smoke.Methods:SD rats were randomly divided into 2 groups:Normal control group (n=4),cigarette smoke(CS) group (n=4). The CS group rats were exposed in the smoke 6 hours/3 days. Hematoxylin-eosin stainingwas used to observe the change of the lung tissue,expression of TGF-β1, CyclinD1 protein were detected by Immunohistochemistry(IHC). Rat alveolar Type Ⅱ epithelial cells(RLE-6TN) were cultured in vitro and stimulated with CSE(four various concentration:0%,0.25%,0.5%,1%) for 48 hours.1% CSE culture medium was used to treat RLE-6TN for 48 hours after RLE-6TN was pretreated by TGF-β1 receptor antagonist(SB431542), cells were randomly divided into 4 groups:control, CSE, SB431542, CSE+SB431542. The cell cycle was detected by flow cytometry instrument. The expression of TGF-β1, CyclinDl protein were detected by ELISA and Western blot.Results:In this study, we observed that the CS can made morphological and pathological changes of rat lung, while CyclinDl expression was decreased(compared with control). We found that CSE significantly caused a time-and dose-dependent increased of G1 phase cells proportion and increased TGF-β1 expression in RLE-6TN, while the expression of CyclinD1 were decreased(P<0.05). Furthermore, treatment of cells with TGF-β1 receptor antagonist activated CyclinDl expression(P<0.05).Conclusion:Take together, CS can made morphological and pathological changes of rat lung. CSE exposure significantly altered the cell cycle, in partly through modifying TGF-β1/CyclinD1 signaling pathways, TGF-β1 plays an important role in this signaling pathway in RLE-6TN.