Abstract

Elevation of intraocular pressure (IOP) is a major, controllable risk factor of primary open-angle glaucoma (POAG). Transforming growth factor-β2 (TGF-β2)-induced excessive accumulation of extracellular matrix (ECM) in the trabecular meshwork (TM) has been demonstrated to contribute significantly to the development of high IOP. We previously showed that treatment with salidroside (Sal), a plant-derived glucoside, can ameliorate the TGF-β2-induced ECM expression in cultured human TM cells and reduce TGF-β2-induced ocular hypertension in mice. In the current study, its underlying molecular mechanism associated with microRNA-210–3p (miR-210–3p) was characterized. We discovered that, in TM tissues of POAG patients , there was an increase in miR-210–3p. And miR-210–3p mediated a portion of the pathological effects of TGF-β2 in vitro (excessive accumulation of ECM in cultured human TM cells) and in vivo (mouse ocular hypertension and ECM accumulation in the TM). Most interestingly, miR-210–3p was down-regulated by Sal, which appeared to mediate a significant portion of its IOP-lowering effect. Thus, these results shed light on the probable molecular mechanisms of TGF-β2 and Sal and indicate that manipulation of miR-210–3p level/activity represents a potential new therapeutic strategy for POAG.