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Dexamethasone, an important anti\u2010inflammatory and immunosuppressant agent, has been widely used in renal disease for decades. Whether it could influence the monocyte and HK\u20102 cell interaction and prevent EMT is still uncertain. In this study, we found that the typical epithelial cell morphology of HK\u20102 cells disappeared 24\u2009h after co\u2010culture with monocytes, and dexamethasone significantly prevented this change in a dose\u2010dependent manner. In addition, we found that dexamethasone prevented monocytes from binding to HK\u20102 cells by inhibiting ICAM\u20101 expression on HK\u20102 cells. Further analysis demonstrated that there was increased E\u2010cadherin expression and decreased \u03b1\u2010SMA and fibronectin expression after co\u2010culture with dexamethasone, suggesting that dexamethasone prevents monocyte\u2010induced HK\u20102 cell transition. The nuclear transcription factor \u03baB (NF\u2010\u03baB) pathway played an important role in this process. These findings suggest a novel mechanism by which corticosteroids may delay the progression of TIF via preventing EMT. J. Cell. Biochem. 114: 632\u2013638, 2013. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24405","type":"journal-article","created":{"date-parts":[[2012,10,11]],"date-time":"2012-10-11T14:50:08Z","timestamp":1349967008000},"page":"632-638","source":"Crossref","is-referenced-by-count":8,"title":["Dexamethasone prevents monocyte\u2010induced tubular epithelial\u2013mesenchymal transition in HK\u20102 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