Abstract
Dexamethasone is a synthetic glucocorticoid that is widely used as an adipogenic inducer in both murine and human in vitro models. Glucocorticoids have been shown to regulate early transcriptional events in adipogenesis. MicroRNAs (miRNAs) have been also implicated in the regulation of preadipocyte differentiation; however, the effects of glucocorticoids on miRNA expression levels during this process have not been studied. In this study we investigated the effects of glucocorticoids on the expression levels of miR-155 in differentiating 3T3-L1 preadipocytes. We found that miR-155 levels were up-regulated (2.4-fold) by glucocorticoids in differentiating 3T3-L1 preadipocytes, and this enhancement was abolished in the presence of RU486, a glucocorticoid receptor antagonist. In contrast, treatment with rosiglitazone, another adipogenic inducer decreased the expression levels of miR-155 in these cells. Further, our data show that endogenous miR-155 is unlikely to be involved in adipogenesis as we show that both dexamethasone and rosiglitazone induced adipogenesis to similar levels. Furthermore, using miR-155 inhibitor, we showed that the dexamethasone mediated miR-155 enhancement did not alter adipogenesis. Our data show that dexamethasone but not rosiglitazone increases miR-155 expression and that the increased expression of miR-155 is not involved in the dexamethasone-mediated adipogenesis in the 3T3-L1 model.
Highlights
Glucocorticoids are a class of corticosteroids that can promote adipogenesis in vivo
We have previously performed a miRNA array experiment to evaluate the specific effects of glucocorticoids on miRNA profiles in differentiating 3T3-L1 preadipocytes that were induced to differentiate for 24 hours in MI (IBMX and insulin) compared to MID (IBMX, insulin, and dexamethasone) conditions
Since dexamethasone treatment led to a robust decrease in the mRNA expressions of suppressor of cytokine signaling (Socs)[1], Socs[3], Fgf[7], and Olfml[3] in differentiating preadipocytes, and we showed that this reduction was inhibited by the glucocorticoid receptor (GR) antagonist RU486, we asked whether this reduction occurred via miR-155
Summary
Glucocorticoids are a class of corticosteroids that can promote adipogenesis in vivo. MiRNAs are small non-coding RNAs that regulate gene expression in different biological processes such as apoptosis, development, and cell proliferation/differentiation[9]. It has been shown that levels of miR-155 were increased both in preadipocytes and adipocytes when cells were treated with tumor necrosis factor (TNF) α13,14. One of these studies suggested that TNF- α mediated increase in endogenous miR-155 supressed 3T3-L1 adipogenesis[13]. In this study we evaluated the role of the dexamethasone-induced endogenous miR-155 in adipogenesis and attempted to elucidate the role of this increase in the differentiation process mediated by glucocorticoids
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