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Induction and Validation of Cellular Senescence in Primary Human Cells
Published on: June 20, 2018
Aging increases p16 INK4a expression in vascular smooth-muscle cells
Luis Rodriguez-Menocal1, Si M Pham, Dania Mateu
1Department of Surgery and Vascular Biology Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Bioscience Reports
|February 7, 2009
Summary
Aging increases p16 INK4a in vascular smooth-muscle cells (VSMCs), potentially heightening blood vessel susceptibility to occlusive diseases. This age-related change in VSMCs may accelerate cardiovascular disease development.
Area of Science:
- Vascular Biology
- Cellular Aging
- Cardiovascular Disease
Background:
- Vascular smooth-muscle cell (VSMC) dysfunction is implicated in atherosclerosis and restenosis.
- Aging is a significant risk factor for cardiovascular diseases.
Purpose of the Study:
- To investigate the hypothesis that aging up-regulates p16 INK4a expression in VSMCs.
- To determine the potential role of increased p16 INK4a in age-related vascular diseases.
Main Methods:
- Primary aortic VSMCs were isolated from young and aged mice.
- Cell proliferation and cell cycle progression were assessed.
- Gene expression of p16 INK4a was analyzed using gene arrays, quantitative RT-PCR, and Western blotting.
- Immunostaining was performed on aortic tissues to quantify p16 INK4a+ cells.
Main Results:
- Aged VSMCs exhibited slower growth and inhibited cell cycle progression compared to young VSMCs.
- A significant 2.5-fold up-regulation of p16 INK4a was observed in VSMCs from aged mice.
- Immunostaining confirmed a higher number of p16 INK4a-positive VSMCs in aged aortas.
Conclusions:
- Aging demonstrably up-regulates p16 INK4a expression in VSMCs, both in culture and within arterial tissue.
- Elevated p16 INK4a in the vasculature during aging may increase susceptibility to vascular occlusive diseases and contribute to cardiovascular disease progression.
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