Aortic & peripheral vascular disease
miR-22 Is a Novel Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation and Neointima Formation
Authors' conclusion
Our data demonstrate that miR-22 and EVI1 are novel regulators of VSMC function, specifically during neointima hyperplasia
Study context
- Population
- Wire-injured mouse femoral arteries; normal and diseased human femoral arteries
- Comparison
- miR-22 overexpression vs miR-22 inhibition
Methodological detailswire-injury mouse model, in vivo, ex vivo and in vitro models, human femoral arteries
- Wire-injury mouse model
- In vivo, ex vivo and in vitro models
- Human femoral arteries
Main finding
As reported in the abstract
- miR-22 expression closely regulated during vascular smooth muscle cell (VSMC) phenotypic modulation
- miR-22 overexpression increased VSMC marker gene expression and inhibited VSMC proliferation and migration; opposite with knockdown
- MECP2 and histone deacetylase 4 (known targets) regulate VSMC phenotypic modulation; EVI1 identified as novel miR-22 target
- miR-22 overexpression in injured vessels reduced target gene expression, decreased VSMC proliferation and inhibited neointima formation; opposite with local miR-22 inhibitor
- Diseased vs healthy human femoral arteries: miR-22 reduced, MECP2 and EVI1 increased; inverse relationship in both
Original publication
miR-22 Is a Novel Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation and Neointima Formation. Circulation. Published 15 December 2017. doi:10.
Summarised from the published abstract; every number is checked against it