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Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
Published on: November 25, 2013
Endothelial cells protect vascular smooth muscle cells from H2O2 attack
1Denver Health Medical Center, Colorado, USA.
The American Journal of Physiology
|June 1, 1997
Summary
Endothelial cells protect vascular smooth muscle cells from oxidant injury via catalase and nitric oxide. This protection is crucial for preventing kidney damage during reperfusion following ischemia.
Area of Science:
- Vascular Biology
- Renal Physiology
- Cellular Toxicology
Background:
- Ischemic acute renal failure alters endothelial-dependent vascular responses.
- Reperfusion oxidants injure renal microvasculature, hindering kidney function recovery.
Purpose of the Study:
- To investigate if endothelial cells (EC) modulate oxidant attack on vascular smooth muscle cells (VSMC).
- To elucidate the mechanisms by which EC protect VSMC from oxidant-induced injury.
Main Methods:
- Coincubation of rat mesenteric artery VSMC with bovine pulmonary artery EC.
- Assessment of VSMC injury via [3H]adenine release following hydrogen peroxide (H2O2) exposure.
- Experimental manipulation of EC with aminotriazole, N omega-nitro-L-arginine (L-NNA), and interleukin-1 beta (IL-1 beta).
Main Results:
- EC significantly reduced H2O2-mediated VSMC injury.
- EC protection was dependent on luminal oxidant exposure and involved catalase activity.
- Nitric oxide (NO) production by EC contributed to the protective effect, which was enhanced by IL-1 beta treatment.
Conclusions:
- Endothelial cells protect VSMC from luminal oxidant attack through catalase- and NO-dependent mechanisms.
- EC dysfunction may contribute to renal injury from oxidants during ischemic kidney reperfusion.
- Targeting EC protective mechanisms could be a therapeutic strategy for ischemic renal injury.
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