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LncRNA SENCR overexpression attenuated the proliferation, migration and phenotypic switching of vascular smooth muscle cells in aortic dissection via the miR-206/myocardin axis
Higher levels of lncRNA SENCR reduce growth, movement, and state changes of blood vessel muscle cells in aortic dissection through the miR-206/myocardin pathway
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Abstract
SENCR overexpression in a mouse model suppressed VSMC proliferation and migration by inhibiting the expression of specific genes.
- SENCR expression was detected in aortic media specimens from aortic dissection patients.
- Increased SENCR levels were associated with reduced vascular smooth muscle cell (VSMC) proliferation and migration.
- SENCR overexpression maintained the contractile phenotype of VSMCs and suppressed aortic media rupture.
- MiR-206 levels decreased with SENCR overexpression, while myocardin levels increased.
- Knockdown of SENCR led to increased VSMC proliferation, migration, and expression of synthetic phenotype-related genes.
- SENCR was shown to regulate miR-206, which directly targets myocardin in VSMCs.
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