Downregulation of SMP30 in senescent human lens epithelial cells

Senescence marker protein 30 (SMP30) has been reported to serve antiapoptotic and antioxidant roles, as well as roles in Ca(2+) regulation, and may be involved in the occurrence and development of cataract. The present study aimed to investigate the expression of SMP30 in senescent human lens epithelial cells (HLECs) and explored the relationship between SMP30 and aging. SRA01/04 cells, a HLEC line, were treated with H(2)O(2) to mimic aging, and cell morphological changes were observed by microscopy and cell activity was examined by MTT assay, senescence-associated-β-galactosidase (SA-β-Gal) staining and cell cycle analysis. The expression of SMP30 mRNA and protein was measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Following prolonged low-dose H(2)O(2) exposure, cells exhibited senescence-related morphological changes, reduced growth activity, increased SA-β-Gal positive staining and cell cycle arrest in the S and G2/M phases. SMP30 mRNA expression levels were significantly downregulated following exposure to 75 and 100 µM H(2)O(2), and the protein expression levels in the same groups were decreased by >6-fold compared with the control untreated cells. However, no significant change was observed in SMP30 expression in the 25 and 50 µM H(2)O(2) exposure groups. These results suggest that, in the early stage of senescence induced by H(2)O(2)-mediated chronic oxidative stress, there may be no significant change in SMP30 expression, but when the oxidative stress increases and senescence is aggravated, SMP30 may be significantly downregulated in the senescent HLECs. The present study indicates that SMP30 may be an important factor involved in the aging process of HLECs and the development of cataract.