The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
LincRNA-p21 Regulates Neointima Formation, Vascular Smooth Muscle Cell Proliferation, Apoptosis, and Atherosclerosis by Enhancing p53 Activity
Open accessAbstract
Background—: Long noncoding RNAs (lncRNAs) have recently been implicated in many biological processes and diseases. Atherosclerosis is a major risk factor for cardiovascular disease. However, the functional role of lncRNAs in atherosclerosis is largely unknown. Methods and Results—: We identified lincRNA-p21 as a key regulator of cell proliferation and apoptosis during atherosclerosis. The expression of lincRNA-p21 was dramatically downregulated in atherosclerotic plaques of ApoE −/− mice, an animal model for atherosclerosis. Through loss- and gain-of-function approaches, we showed that lincRNA-p21 represses cell proliferation and induces apoptosis in vascular smooth muscle cells and mouse mononuclear macrophage cells in vitro. Moreover, we found that inhibition of lincRNA-p21 results in neointimal hyperplasia in vivo in a carotid artery injury model. Genome-wide analysis revealed that lincRNA-p21 inhibition dysregulated many p53 targets. Furthermore, lincRNA-p21, a transcriptional target of p53, feeds back to enhance p53 transcriptional activity, at least in part, via binding to mouse double minute 2 (MDM2), an E3 ubiquitin-protein ligase. The association of lincRNA-p21 and MDM2 releases MDM2 repression of p53, enabling p53 to interact with p300 and to bind to the promoters/enhancers of its target genes. Finally, we show that lincRNA-p21 expression is decreased in patients with coronary artery disease. Conclusions—: Our studies identify lincRNA-p21 as a novel regulator of cell proliferation and apoptosis and suggest that this lncRNA could serve as a therapeutic target to treat atherosclerosis and related cardiovascular disorders.
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Cites
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BackgroundLong Noncoding RNA as Modular Scaffold of Histone Modification Complexes
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Method
Cited by
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Noncoding RNAs regulate NF-κB signaling to modulate blood vessel inflammation
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Metadata
- Authors
- Wu, G., Cai, J., Han, Y., Chen, J., Huang, Z.-P., Chen, C., Cai, Y., Huang, H., Yang, Y., Liu, Y., Xu, Z., He, D., Zhang, X., Hu, X., Pinello, L., Zhong, D., He, F., Yuan, G.-C., Wang, D.-Z., & Zeng, C.
- Venue
- Circulation
- Published
- 2014-10-21
- Volume
- 130
- Issue
- 17
- Pages
- 1452-1465
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2054542819
- Cited by
- 485
- References
- 53
- FWCI
- 14.91
- Type
- journal article
- Language
- en
- Open access
- green
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- Wu, G., Cai, J., Han, Y., Chen, J., Huang, Z.-P., Chen, C., Cai, Y., Huang, H., Yang, Y., Liu, Y., Xu, Z., He, D., Zhang, X., Hu, X., Pinello, L., Zhong, D., He, F., Yuan, G.-C., Wang, D.-Z., & Zeng, C. (2014). LincRNA-p21 Regulates Neointima Formation, Vascular Smooth Muscle Cell Proliferation, Apoptosis, and Atherosclerosis by Enhancing p53 Activity. Circulation. https://doi.org/10.1161/circulationaha.114.011675
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