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Elastin in systemic and pulmonary hypertension
1Division of Cardiovascular Research, Hospital for Sick Children, Toronto, Ontario, Canada.
Ciba Foundation Symposium
|January 1, 1995
Summary
Hypertension causes increased elastin in blood vessels, reinforcing the condition. Novel mechanisms and potential therapies targeting elastin turnover are being explored to reverse these persistent vascular changes.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Elevated vascular wall stress in hypertension triggers rapid elastin production and accumulation.
- These structural changes, while initially protective, can perpetuate hypertension long-term.
- Mechanisms beyond elastin gene expression, like enhanced translation or matrix accumulation, are implicated.
Purpose of the Study:
- To investigate the mechanisms of stretch-induced elastin synthesis in hypertension.
- To explore the role of signaling pathways in elastin accumulation.
- To identify potential therapeutic strategies for reversing vascular elastin buildup.
Main Methods:
- Utilized in vitro organ and cell culture models.
- Investigated the involvement of phospholipases and protein kinases (e.g., protein kinase C).
- Examined tyrosine phosphorylation of key signaling molecules like focal adhesion kinase and lipocortin family members.
Main Results:
- Stretch-induced elastin synthesis involves phospholipases and protein kinases.
- Tyrosine phosphorylation of sensors, including focal adhesion kinase, is crucial for signal transduction.
- Accumulated elastin persists post-hypertension due to slow turnover, impacting vessel properties.
Conclusions:
- Novel mechanisms regulate elastin synthesis and accumulation in hypertension.
- Understanding these pathways offers targets for therapeutic intervention.
- Promoting elastin turnover via endogenous enzymes may reverse pathological vascular remodeling.