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Objective:  Evidence suggests that pioglitazone improves the function of endothelial progenitor cells (EPCs). However, the knowledge of its molecular mechanism remains limited. In the present study, the role of long non-coding RNA MATAL1 in modulating the number and function of EPCS in type 2 diabetes mellitus (T2DM) was characterized. Methods : Circulating EPCs were obtained from peripheral blood of healthy subjects and T2DM patients with or without pioglitazone treatment. The in vitro  experiments were conducted in bone marrow-EPCs to evaluate the effect of pioglitazone and its possible mechanism. Results : Pioglitazone increased circulating EPCs number and improved their function in T2DM patients. Transfected EPCs with siRNA-MALAT1, the increase of c-Myc protein expression induced by pioglitazone treatment was canceled. In db/db diabetic mice, a glucose tolerance test showed that pioglitazone increased glucose tolerance, which was reversed by siRNA-MALAT1. Conclusion : Pioglitazone improves the EPCs function possibly through regulating MALAT1 and c-Myc expression in T2DM. Keywords: pioglitazone; diabetes mellitus; MALAT1; endothelial function; glucose tolerant

aging pathobiology and therapeutics

Pioglitazone up-regulates MALAT1 and promotes the proliferation of endothelial progenitor cells through increasing c-Myc expression in type 2 diabetes mellitus