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[Expression and antagonist role of endothelin and nitric oxide synthase in atherosclerotic plaque]
Objective:
To study the pathogenetic mechanism of atherosclerotic plaque, the action of mediation and antagonism of endothelin (ET) and nitric oxide synthase (NOS) was investigated.
Methods:
In situ hybridization, RT-PCR on endothelin and NOS, cytochemistry on NOS were measured using the rabbit atherosclerosis model and cultured vascular smooth muscle cells (VSMC) from normal rabbit.
Results:
Transcription of endothelin mRNA increased and transcription of NOS mRNA decreased in astherosclerotic plaque: compared with normal aorta, expression of ET gene in plaque was increased by 1.2 times and the expression of NOS gene was decreased by 22.2%; cytochemistry combined with image pattern analysis showed that ET could inhibit NOS protien synthesis in VSMC; type A receptor antagonist of ET could inhibit the role of ET which causes a decrease of NOS protein in VSMC.
Conclusion:
The imbalance between NOS and ET, namely abnormal increase of ET and/or obvious decrease of NOS, is related to atherosclerotic plaque formation.
Insights
Atherosclerotic plaque formation is linked to an imbalance between endothelin (ET) and nitric oxide synthase (NOS). Increased ET and decreased NOS expression contribute to this condition.
Area of Science:
- Cardiovascular Biology
- Molecular Pathology
Context:
- Atherosclerosis is a complex disease involving plaque buildup in arteries.
- Endothelin (ET) and nitric oxide synthase (NOS) play critical roles in vascular function and homeostasis.
Purpose:
- To investigate the pathogenetic mechanism of atherosclerotic plaque.
- To study the interplay between endothelin (ET) and nitric oxide synthase (NOS) in atherosclerosis.
Summary:
- Studies show increased endothelin mRNA and decreased nitric oxide synthase mRNA in atherosclerotic plaques.
- Endothelin inhibits nitric oxide synthase protein synthesis in vascular smooth muscle cells (VSMC).
- ET receptor antagonists can block endothelin's inhibitory effect on NOS protein.
Impact:
- Findings suggest that an imbalance favoring ET over NOS contributes to atherosclerotic plaque formation.
- This research highlights potential therapeutic targets for managing atherosclerosis by modulating ET and NOS pathways.