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Inhibitory effect of Trichostatin A in transformation growth factor ©¬1-induced epithelial-mesenchymal transition in A549 cell
°í·Á´ëÇб³ ÀÇ°ú´ëÇÐ À̺ñÀÎÈÄ-µÎ°æºÎ¿Ü°úÇÐ ±³½Ç©ö, °í·Á´ëÇб³ ´ëÇпø ÀÇ°úÇаú©÷
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¸ñÀû: Tissue remodeling is a common finding in all types of chronic inflammatory diseases of upper airways including asthma, chronic obstructive pulmonary disease and chronic rhinosinusitis. The aim of this study was to study the effect of Trichostatin A on TGF-¥â1-induced epithelial-mesenchymal transition in A549 cells. ¹æ¹ý:A549 cells were exposed to TSA prior to stimulation with TGF-¥â1. Expression levels of E-cadherin, vimentin, fibronectin, ¥á-SMA, HDAC2 and HDAC4 were determined by western blot and/or immunofluorescent staining. Hyperacetylation of histone H2 and H4 by TSA was measured by western blot analysis with nucleic protein. After siControl or siHDAC transfection, effects of HDAC2 and HDAC4 silencing on expression of E-cadherin, vimentin, fibronectin, ¥á-SMA, HDAC2 and HDAC4 in TGF-¥â1-induced A549 was determined by RT-PCR and/or western blot. °á°ú:In TGF-¥â-1–induced A549 cells, TSA significantly inhibited the expressions of vimentin, fibronectin, ¥á-SMA, HDAC2 and HDAC4 and stimulated the expression of E-cadherin. TSA induced hyperacetylation of histone. HDAC2 and HDAC4 silencing inhibited expression of vimentin, fibronectin, ¥á-SMA, HDAC2 and HDAC4. °á·Ð:We showed that histone acetylation is associated with epithelial-mesenchymal transition in A549 cells. The results of our study suggested that TSA is a possible candidate for suppression of tissue remodeling in airway.


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