LincRNA-p21 regulates neointima formation, vascular smooth muscle cell proliferation, apoptosis, and atherosclerosis by enhancing p53 activity
- Gengze Wu 1,2, Jin Cai 1, Yu Han 1, Jinghai Chen 2, Zhan-Peng Huang 2, Caiyu Chen 1, Yue Cai 1, Hefei Huang 1, Yujia Yang 1, Yukai Liu 1, Zaicheng Xu 1, Duofen He 1, Xiaoqun Zhang 1, Xiaoyun Hu 2, Luca Pinello 3, Dan Zhong 4, Fengtian He 4, Guo-Cheng Yuan 3, Da-Zhi Wang 2,5, Chunyu Zeng 1
- 1Department of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
- 2Department of Cardiology, Boston Children's Hospital, Harvard Medical School, Boston, MA.
- 3Department of Biostatistics and Computational Biology, Dana-Farber Cancer Institute and Harvard School of Public Heath, Boston, MA.
- 4Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, China.
- 5Harvard Stem Cell Institute, Harvard University, Cambridge, MA.
- 0Department of Cardiology, Chongqing Institute of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, China.
Related Experiment Videos
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Long noncoding RNA p21 (lincRNA-p21) regulates cell proliferation and apoptosis in atherosclerosis. Its downregulation in plaques suggests lincRNA-p21 as a potential therapeutic target for cardiovascular diseases.
Area Of Science
- Molecular Biology
- Genetics
- Cardiovascular Research
Background
- Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in biological processes and diseases.
- Atherosclerosis, a primary contributor to cardiovascular disease, has an incompletely understood lncRNA involvement.
- Investigating lncRNAs in atherosclerosis is crucial for understanding disease mechanisms.
Purpose Of The Study
- To identify and characterize the role of specific lncRNAs in the pathogenesis of atherosclerosis.
- To elucidate the regulatory mechanisms of lincRNA-p21 in vascular cells.
- To evaluate lincRNA-p21 as a potential therapeutic target for atherosclerosis.
Main Methods
- Utilized ApoE(-/-) mice as an atherosclerosis model.
- Employed loss- and gain-of-function studies in vascular smooth muscle and macrophage cells.
- Performed in vivo carotid artery injury model to assess neointimal hyperplasia.
- Conducted genome-wide analysis to identify p53 target genes.
- Investigated the interaction between lincRNA-p21, p53, and MDM2.
Main Results
- Identified lincRNA-p21 as a key regulator of cell proliferation and apoptosis in atherosclerosis.
- Observed significantly downregulated lincRNA-p21 expression in atherosclerotic plaques.
- Demonstrated that lincRNA-p21 represses proliferation and induces apoptosis in vascular cells.
- Showed that lincRNA-p21 inhibition leads to neointimal hyperplasia in vivo.
- Revealed that lincRNA-p21 enhances p53 transcriptional activity by interacting with MDM2.
- Found decreased lincRNA-p21 expression in patients with coronary artery disease.
Conclusions
- lincRNA-p21 is a novel regulator of cell proliferation and apoptosis in the context of atherosclerosis.
- lincRNA-p21 plays a protective role by suppressing vascular cell proliferation and promoting apoptosis.
- lincRNA-p21 represents a promising therapeutic target for atherosclerosis and associated cardiovascular diseases.
Related Experiment Videos
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.