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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
Published on: February 16, 2015
ACE inhibition actively promotes cell survival by altering gene expression
Hamdi K Hamdi1, Raquel Castellon
1Department of Ophthalmology, University of California-Irvine, Irvine, CA, USA. hhamdi@uci.edu
Biochemical and Biophysical Research Communications
|October 16, 2003
Summary
Angiotensin-converting enzyme (ACE) inhibition with captopril significantly enhances endothelial cell (EC) survival and delays apoptosis in cell culture. This ACE inhibition strategy offers a novel approach to improving endothelial cell viability and function.
Area of Science:
- Ophthalmology
- Cell Biology
- Pharmacology
Background:
- Endothelial cells (EC) in the retina and choroid are crucial for ocular health.
- Understanding factors that promote EC survival is vital for treating ocular diseases.
- Apoptosis, or programmed cell death, is a key mechanism in EC dysfunction.
Purpose of the Study:
- To investigate the impact of angiotensin-converting enzyme (ACE) inhibition on the survival of bovine retinal (REC) and choroidal (CEC) endothelial cells (EC).
- To elucidate the molecular mechanisms underlying ACE inhibition-mediated EC survival.
Main Methods:
- Cell culture of bovine REC and CEC.
- Treatment with the ACE inhibitor captopril.
- Induction of cell stress via slow starvation.
- Assessment of cell viability and apoptosis using morphological and molecular markers.
- Gene expression analysis using RT-PCR to identify changes in survival and growth-related proteins.
- Inhibition of urokinase plasminogen activator (uPA) with amiloride to assess its role.
Main Results:
- Captopril treatment significantly delayed apoptotic tube collapse in REC on Matrigel for over 15 days.
- Captopril increased EC viability by approximately 200% after prolonged culture and starvation.
- Vehicle-treated EC exhibited apoptotic features, while captopril-treated EC did not.
- Captopril modulated the expression of pro-survival (mortalin-2, uPA, uPAR) and anti-growth (sprouty-4, tPA) genes in REC.
- Captopril also affected tPA and PAI-1 expression in CEC.
- Amiloride blocked the captopril-induced increase in EC survival, sprouting, and invasion.
Conclusions:
- ACE inhibition, specifically with captopril, confers significant pro-survival effects on retinal and choroidal endothelial cells.
- The protective mechanism involves the upregulation of pro-survival genes and downregulation of anti-growth factors.
- Captopril's effects are partly mediated through the uPA pathway.
- ACE inhibition represents a promising strategy for enhancing endothelial cell survival and potentially treating ocular vascular conditions.
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