Original Article PDGF-Rb and microRNA-329 are associated with endometrial dysfunctionvia targeting CD146

* Equal contributors. Received October 30, 2015; Accepted December 26, 2015; Epub February 1, 2016; Published February 15, 2016 Abstract: It is believed that endometrial miRNAs contribute to the etiology of endometrial dysfunction, however, the mechanisms remain unclear. Here we collected endometrial tissues from infertility patients with different thickness and characterized the miRNA expression profiles of these three groups. MiR-329 was dramatically down-regulated in infertility patients with endometrial hyperplasia. In addition, we found that miR-329 overexpression could inhibit CD146 expression in ESCs, which is a marker and is mainly expressed in the cytoplasm of ESCs. Moreover, bioinfor- matics analysis suggested that miR-329 was a regulator of CD146. Importantly, up-regulation of miR-329 in ESCs decreased cell proliferation, migration and invasion, and the underlying mechanism was mediated, at least partially, through the suppression of CD146 expression. Furthermore, PDGF increased cell viability, migration and invasion in a dose-dependent manner, PDGF-Rb antagonist, imatinib, could reverse PDGF-induced ESCs dysfunction through the activation of PDGF/PDGF-Rb-dependent signaling pathways. In conclusion, PDGF-Rb could play an important role in endometrial hyperplasia, and miR-329 via targeting CD146 associated with endometrial dysfunction and might be a potential therapeutic target against endometrial hyperplasia.