Related Experiment Videos
Periadventitial inducible nitric oxide synthase expression and intimal thickening
G R De Meyer1, M M Kockx, K M Cromheeke
1Divisions of Pharmacology, University of Antwerp, Belgium. gdemeyer@uia.ua.ac.be
Arteriosclerosis, Thrombosis, and Vascular Biology
|August 11, 2000
Summary
Inducible nitric oxide synthase (iNOS) is not found in the intimal thickening of arteries but is present in surrounding tissues. Inhibiting iNOS accelerates intimal thickening, suggesting a protective role against this process.
Area of Science:
- Vascular Biology
- Immunology
- Biochemistry
Background:
- Intimal thickening is a key feature of vascular disease.
- The role of inducible nitric oxide synthase (iNOS) in intimal thickening is not fully understood.
Purpose of the Study:
- To investigate the localization of iNOS during carotid artery intimal thickening.
- To determine the effect of iNOS inhibition on intimal thickness.
- To examine the impact of oxidized LDL (ox-LDL) on iNOS expression.
Main Methods:
- Rabbit carotid artery model with silicone collar placement.
- Immunohistochemistry for iNOS localization.
- Reverse transcription-polymerase chain reaction for iNOS mRNA.
- Local delivery of iNOS inhibitor (L-NIL) or saline via osmotic minipumps.
- Oxidized LDL infusion.
Main Results:
- iNOS was localized in macrophages and T lymphocytes in the adventitia and periadventitia, not in the intima or media.
- iNOS mRNA was detected in collared arteries.
- Inhibition of iNOS significantly increased intimal thickness and nitrotyrosine staining.
- Ox-LDL induced intimal thickening with iNOS-positive immune cell infiltration.
Conclusions:
- iNOS is expressed in perivascular immune cells and appears to counteract intimal thickening.
- iNOS inhibition exacerbates intimal thickening, highlighting its protective role.
- Ox-LDL promotes inflammation and intimal thickening, with iNOS present in infiltrating immune cells.