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Gestational diabetes mellitus (GDM) is a metabolic disorder whose major pathophysiological basis is demonstrated as placental insulin resistance (IR), while Smad4 always functions in the signal transduction of transforming growth factor beta (TGF-β) pathway. Our study aims to figure out the role of Smad4 in an insulin resistance (IR) cellular model using placental trophoblast cell line. Importantly, HTR8-Svneo cells, in the status of IR, indicated a significant increase in the expression of Smad4. Subsequently, the HTR8-Svneo cell line with up-regulated or depleted Smad4 was respectively achieved by the effective over-expressed plasmid or siRNA of Smad4. We found out that the deficiency of Smad4 could promote the insulin sensitivity and restrict the inflammatory response in IR group of cells with significant augment in glucose uptake, up-regulation of insulin signalling-related molecules and attenuation in inflammatory biomarker expressions. On the contrary, the over-expression of Smad4 showed a reversal effect on these alterations in IR group of cells. Besides, the positive effect of Smad4 on cell viability was also observed in our study. SIGNIFICANCE OF THE STUDY: Gestational diabetes mellitus (GDM) is a metabolic disorder whose major pathophysiological basis is demonstrated as insulin resistance (IR). Importantly, our findings indicate that the deficiency of Smad4 significantly improves the insulin sensitivity and relieves the inflammation in the cellular model of IR. Besides, the positive effect of Smad4 on cell viability was also observed in our study. Our present findings provide novel insights for the investigation on molecular details about the GDM pathogenesis.
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Cell_biochemistry_and_function
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The role of Smad4 in the regulation of insulin resistance, inflammation and cell proliferation in HTR8-Svneo cells.
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