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MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1
Open accessAbstract
Atherosclerosis, a hyperlipidemia-induced chronic inflammatory process of the arterial wall, develops preferentially at sites where disturbed laminar flow compromises endothelial cell (EC) function. Here we show that endothelial miR-126-5p maintains a proliferative reserve in ECs through suppression of the Notch1 inhibitor delta-like 1 homolog (Dlk1) and thereby prevents atherosclerotic lesion formation. Endothelial recovery after denudation was impaired in Mir126−/− mice because lack of miR-126-5p, but not miR-126-3p, reduced EC proliferation by derepressing Dlk1. At nonpredilection sites, high miR-126-5p levels in endothelial cells confer a proliferative reserve that compensates for the antiproliferative effects of hyperlipidemia, such that atherosclerosis was exacerbated in Mir126−/− mice. In contrast, downregulation of miR-126-5p by disturbed flow abrogated EC proliferation at predilection sites in response to hyperlipidemic stress through upregulation of Dlk1 expression. Administration of miR-126-5p rescued EC proliferation at predilection sites and limited atherosclerosis, introducing a potential therapeutic approach.
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Metadata
- Authors
- Schober, A., Nazari-Jahantigh, M., Wei, Y., Bidzhekov, K., Gremse, F., Grommes, J., Megens, R. T. A., Heyll, K., Noels, H., Hristov, M., Wang, S., Kiessling, F., Olson, E. N., & Weber, C.
- Venue
- Nature Medicine
- Published
- 2014-03-02
- Volume
- 20
- Issue
- 4
- Pages
- 368-376
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- OpenAlex
- W2148937727
- Cited by
- 630
- References
- 50
- FWCI
- 19.34
- Type
- journal article
- Language
- en
- Open access
- green
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