Aortic & peripheral vascular disease
INKILN is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10
Authors' conclusion
These findings elucidate an important pathway of VSMC inflammation involving an INKILN/MKL1/USP10 regulatory axis.
Study context
- Population
- Human vascular smooth muscle cell (VSMCs), ex vivo vessels, human atherosclerosis and AAA, BAC transgenic mice
Main finding
As reported in the abstract
- INKILN downregulated in contractile VSMCs and induced in human atherosclerosis and AAA
- INKILN transcriptionally activated by the p65 pathway, partially via a predicted NF-κB site in its proximal promoter
- INKILN activates proinflammatory gene expression in cultured human VSMCs and ex vivo cultured vessels
- INKILN physically interacts with and stabilizes MKL1
- INKILN depletion blocks interleukin-1β-induced nuclear localization of p65 and MKL1
- INKILN knockdown abolishes p65–MKL1 interaction and NF-κB reporter luciferase activity
- INKILN knockdown enhances MKL1 ubiquitination via reduced interaction with USP10
- INKILN induced in injured carotid arteries and exacerbates ligation injury-induced neointimal formation in BAC transgenic mice
Original publication
INKILN is a Novel Long Noncoding RNA Promoting Vascular Smooth Muscle Inflammation via Scaffolding MKL1 and USP10. Circulation. Published 18 May 2023. doi:10.
Summarised from the published abstract; every number is checked against it