ArticleMolecular medicine reports2017
Downregulation of SMP30 in senescent human lens epithelial cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Cellular Senescence of Lens Epithelial Cells and Age-Related Cataract: A Systematic Review.Bioengineering (Basel, Switzerland) · 2026Review
- SMP30 May protect human lens epithelial cells against high glucose-induced oxidative damage by regulating the Keap1/Nrf2/NQO1 pathway.Scientific reports · 2025Article
- SMP30 Attenuates Lens Epithelial Cells Pyroptosis of Cataract via the Downregulation of p-STAT3.Journal of inflammation research · 2025Article
- Potential immune involvement in cataract: from mechanisms to future scope of therapies.International journal of ophthalmology · 2025Review
- Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function.Bioengineered · 2022Article
- New Evidence on Regucalcin, Body Composition, and Walking Ability Adaptations to Multicomponent Exercise Training in Functionally Limited and Frail Older Adults.International journal of environmental research and public health · 2021Article
- Carbofuran accelerates the cellular senescence and declines the life span of spns1 mutant zebrafish.Journal of cellular and molecular medicine · 2021Article
- Blast Exposure Leads to Accelerated Cellular Senescence in the Rat Brain.Frontiers in neurology · 2020Article
- Article
- Cellular senescence: a view throughout organismal life.Cellular and molecular life sciences : CMLS · 2018Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence marker protein 30 (SMP30) has been reported to serve antiapoptotic and antioxidant roles, as well as roles in Ca2+ 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 H2O2 to mimic aging, and cell morphological changes were observed by microscopy and cell activity was exami-ned 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 H2O2 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 H2O2, 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 H2O2 exposure groups. These results suggest that, in the early stage of senescence induced by H2O2‑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.
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