Altered lncRNAs Transcriptomic Profiles in Atherosclerosis-Induced Ischemic Stroke.


Journal

Cellular and molecular neurobiology
ISSN: 1573-6830
Titre abrégé: Cell Mol Neurobiol
Pays: United States
ID NLM: 8200709

Informations de publication

Date de publication:
Jan 2022
Historique:
received: 11 03 2020
accepted: 05 07 2020
pubmed: 13 7 2020
medline: 1 4 2022
entrez: 13 7 2020
Statut: ppublish

Résumé

Long non-coding RNAs (lncRNAs) can not only regulate gene transcription and translation, but also participate in the development of central nervous system diseases as epigenetic modification factors. However, their functional significance in atherosclerosis-induced ischemic stroke (AIIS) is unclear. The study aimed to screen out differentially expressed lncRNAs (delncRNAs), and to elucidate their potential regulatory mechanisms in the pathophysiology of AIIS. Based on the clinicopathological features and clinical images, we screened out 10 patients with AIIS and recruited 10 healthy volunteers. Then we used microarray to detect the whole blood RNA of subjects, and explored the biological functions of delncRNAs by GO and KEGG analysis. After further analyzing the delncRNAs of THP-1 stimulated with ox-LDL, selective lncRNAs were screened and a corresponding lncRNA-mRNA interaction network was constructed through co-expression analysis. We yielded 180 delncRNAs (44 up-regulated and 136 down-regulated) and 218 demRNAs (45 up-regulated and 173 down-regulated). Lnc-SCARNA8 and lnc-SNRPN-2 are the most significant elevated and decreased lncRNA in AIIS, respectively. The delncRNAs may play a significant role in ubiquitination-mediated protein degradation signaling pathways. According to lncRNA-mRNA network, the expression of vacuolar protein sorting 13 homolog B (VPS13B) and biliverdin reductase B (BLVRB) were significantly regulated. Our findings suggest that the ubiquitinated proteasome pathway, VPS13B and BLVRB may play a fundamental role in the pathological process of AIIS.

Identifiants

pubmed: 32653974
doi: 10.1007/s10571-020-00918-y
pii: 10.1007/s10571-020-00918-y
doi:

Substances chimiques

RNA, Long Noncoding 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

265-278

Subventions

Organisme : National Natural Science Foundation of China
ID : 81571134
Organisme : National Natural Science Foundation of China
ID : 81973512

Informations de copyright

© 2020. Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Wenchen Ruan (W)

Department of Neurology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, People's Republic of China.
State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.

Jiayang Wu (J)

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China.

Jingjing Su (J)

Department of Neurology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, People's Republic of China.

Yongcheng Jiang (Y)

Department of Neurology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, People's Republic of China.

Tao Pang (T)

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Drug Screening, China Pharmaceutical University, #24 Tong Jia Xiang Street, Nanjing, 210009, People's Republic of China. tpang@cpu.edu.cn.

Jingwei Li (J)

Department of Neurology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, People's Republic of China. ljw323@yeah.net.

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