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Different vasculoprotective roles of NO synthase isoforms in vascular lesion formation in mice
K Yogo1, H Shimokawa, H Funakoshi
1Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Abstract:
NO is known to have several important vasculoprotective actions. Although NO is synthesized by 3 different NO synthase (NOS) isoforms, the vasculoprotective action of individual NOS isoforms remains to be clarified. Permanent ligation of the left common carotid artery was performed in control, endothelial NOS (eNOS) knockout (eNOS-KO), and inducible NOS (iNOS) knockout (iNOS-KO) mice. Four weeks after the procedure, neointimal formation and reduction of cross-sectional vascular area (constrictive remodeling) were noted in the left carotid artery. In the eNOS-KO mice, the extent of neointimal formation was significantly larger than in the control or iNOS-KO mice, whereas the extent of vascular remodeling was the highest in the iNOS-KO mice compared with other 2 strains. Antiplatelet therapy with aspirin or antihypertensive treatment with bunazosin failed to inhibit the accelerated neointimal formation in the eNOS-KO mice. These results indicate that eNOS and iNOS have different vasculoprotective actions against the vascular lesion formation caused by blood flow disruption in vivo: NO derived from eNOS inhibits neointimal formation, whereas NO derived from iNOS suppresses the development of constrictive remodeling.
Insights
Nitric oxide (NO) from endothelial NO synthase (eNOS) prevents artery thickening, while NO from inducible NO synthase (iNOS) reduces vascular constriction. These distinct roles highlight specific vasculoprotective actions in response to injury.
Area of Science:
- Cardiovascular Biology
- Vascular Physiology
- Nitric Oxide Signaling
Background:
- Nitric oxide (NO) exerts crucial vasculoprotective effects.
- Three nitric oxide synthase (NOS) isoforms exist, but their individual roles in vascular protection are not fully understood.
Purpose of the Study:
- To elucidate the distinct vasculoprotective functions of endothelial NOS (eNOS) and inducible NOS (iNOS) in vivo.
- To investigate the impact of eNOS and iNOS deficiency on vascular lesion formation following arterial ligation.
Main Methods:
- Permanent ligation of the left common carotid artery in control, eNOS knockout (eNOS-KO), and iNOS knockout (iNOS-KO) mice.
- Assessment of neointimal formation and vascular remodeling (constrictive remodeling) four weeks post-ligation.
- Evaluation of therapeutic interventions including antiplatelet and antihypertensive treatments.
Main Results:
- eNOS-KO mice exhibited significantly greater neointimal formation compared to controls and iNOS-KO mice.
- iNOS-KO mice showed the most pronounced constrictive remodeling.
- Neither aspirin nor bunazosin treatment mitigated the accelerated neointimal formation in eNOS-KO mice.
Conclusions:
- Endothelial NOS (eNOS)-derived NO plays a key role in inhibiting neointimal hyperplasia.
- Inducible NOS (iNOS)-derived NO is critical for suppressing constrictive vascular remodeling.
- eNOS and iNOS possess distinct, non-redundant vasculoprotective actions against vascular injury.
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