Hsp70 protects human trabecular meshwork cells injury induced by UVB through Smad pathway.

AIM: Glaucoma is a universal eye disease which is commonly associated with increased intraocular pressure caused by impaired aqueous humor (AH) drainage. This study aimed to investigate the effects of Hsp70 on trabecular meshwork (TM) injury induced by UVB.

METHODS: Real-time quantitative PCR (qRT-PCR) was used to examine the mRNA levels of Hsp70. siRNA was used to downregulate Hsp70 expression in the TM cells to inspect changes in cell proliferation and apoptosis. Cell proliferation was assessed by a Cell Counting Kit-8 (CCK-8) assay and the number of apoptotic cells was assessed using annexin V-FITC/PI apoptosis detection kit. The Smad signaling pathway was investigated using western blotting analyses.

RESULTS: The overexpression of Hsp70 promoted cell proliferation and suppressed apoptosis. What's more, the overexpression of Hsp70 suppressed the expression of Smad-2, Smad-3 and Smad-7.

CONCLUSION: Hsp70 might improve cell viability and inhibit TM apoptosis by inhibition of the Smad pathway. Hsp70 is a potential therapeutic target for the treatment of glaucoma.