Smad7 siRNA inhibit expression of extracellular matrix in trabecular meshwork cells treated with TGF-β2.

Extracellular matrix (ECM) deposits lead to elevated resistance of aqueous humor outflow which play an important role in the development of primary open angle glaucoma (POAG). The TGF-β2 (transforming growth factor β)/Smad (signaling mathers against decapentaplegic) pathway is known to regulate the ECM deposits. In this study, we determined the effect of Smad7 siRNA transfection in inhibiting the expression of ECM components. Plasmid containing Smad7 siRNA was used to transfect cultured human trabecular meshwork cells (HTM). Protein expression of Smad7, fibronectin, and laminin was determined using western blot. Downregulation of Smad7 interrupts the effects of TGF-β2 on the expression of several ECM components. Smad7 siRNA can partially decrease the expression of Smad7, fibronectin, and laminin. Smad7 plays an important role in regulating the ECM protein in the aqueous outflow pathway.