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Induction and Validation of Cellular Senescence in Primary Human Cells
Published on: June 20, 2018
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P38-Mediated Cellular Senescence in Conjunctivochalasis Fibroblasts
Minhong Xiang1, Lijuan Mo1, Yueping Zhan1
1Department of Ophthalmology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Investigative Ophthalmology & Visual Science
|November 5, 2019
Summary
Cellular senescence contributes to conjunctivochalasis (CCH) progression. Blocking p38 signaling reduces senescence, reactive oxygen species, and improves cell viability in CCH fibroblasts.
Area of Science:
- Ophthalmology
- Cell Biology
- Aging Research
Background:
- Conjunctivochalasis (CCH) is a prevalent ocular condition with largely unknown pathogenesis.
- CCH disproportionately affects older individuals, suggesting a link to age-related cellular changes.
Purpose of the Study:
- To investigate the role of cellular senescence in the progression of conjunctivochalasis (CCH).
- To elucidate the underlying molecular mechanisms, particularly the involvement of p38 signaling, in CCH-related cellular senescence.
Main Methods:
- Compared conjunctival tissues from CCH patients and healthy controls using SA-β-Gal staining and qRT-PCR for senescence markers (p53, p21) and p38.
- Utilized siRNA targeting p38 (siP38) and a p38 inhibitor (SB203580) in CCH fibroblasts to assess effects on senescence, cell viability, and ROS production.
Main Results:
- CCH tissues exhibited significantly higher SA-β-Gal-positive cells and elevated expression of p53, p21, and p38 compared to controls.
- Inhibition of p38 signaling in CCH fibroblasts led to reduced senescence, decreased ROS, enhanced cell viability, and lower p53/p21 expression.
Conclusions:
- Cellular senescence is a potential causative factor in conjunctivochalasis (CCH).
- The p38 signaling pathway plays a crucial role in promoting cellular senescence in CCH fibroblasts, likely through the p53/p21 pathway.
