Characterization of Long Noncoding RNA and mRNA Profiles in Sepsis-Induced Myocardial Depression.

Pvt1 lncRNA myocardial depression sepsis transcriptome

Journal

Molecular therapy. Nucleic acids
ISSN: 2162-2531
Titre abrégé: Mol Ther Nucleic Acids
Pays: United States
ID NLM: 101581621

Informations de publication

Date de publication:
06 Sep 2019
Historique:
received: 10 04 2019
revised: 23 07 2019
accepted: 24 07 2019
pubmed: 1 9 2019
medline: 1 9 2019
entrez: 1 9 2019
Statut: ppublish

Résumé

Septic shock with heart dysfunction is very common in intensive care units. However, whether long noncoding RNA (lncRNA) and mRNA profiles differ between patients with and without myocardial depression is unknown. We generated rat models of hypodynamic septic shock induced by lipopolysaccharide. A total of 12 rat models was constructed and heart tissue from each was collected. Whole genomic RNA sequencing was performed on left ventricular tissue; 6,508 novel lncRNAs and 432 annotated lncRNAs were identified in heart samples, and 74 lncRNAs were expressed differently in the sepsis and control groups. Gene ontology term enrichment indicated apoptosis and its related pathways showed obvious enrichment, which suggested cell apoptosis could play a critical role in the process of myocardial depression. Furthermore, we focused on one lncRNA from the Pvt1 gene. By silencing this lncRNA, we demonstrated knockdown of Pvt1 expression could induce cell apoptosis in lipopolysaccharide-induced heart cells, through increasing the expression of c-Myc, Bid, Bax, and caspase-3 and decreasing the expression of Myd88 and Bcl-2, thereby proving its functional role in myocardial depression. These results demonstrate that lncRNAs both participate in and mediate the pathological process of myocardial depression. Our study improves the understanding of the basic molecular mechanisms underlying myocardial depression.

Identifiants

pubmed: 31472370
pii: S2162-2531(19)30210-0
doi: 10.1016/j.omtn.2019.07.020
pmc: PMC6722300
pii:
doi:

Types de publication

Journal Article

Langues

eng

Pagination

852-866

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL131952
Pays : United States

Informations de copyright

Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

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Auteurs

Tie-Ning Zhang (TN)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Julie E Goodwin (JE)

Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA; Department of Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA.

Bing Liu (B)

Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA; Department of Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA.

Da Li (D)

Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, China.

Ri Wen (R)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Ni Yang (N)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Jing Xia (J)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Han Zhou (H)

Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA; Department of Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA.

Tao Zhang (T)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Wen-Liang Song (WL)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China.

Chun-Feng Liu (CF)

Department of Pediatrics, PICU, Shengjing Hospital of China Medical University, Shenyang, Liaoning Province, 110004, China. Electronic address: zhliu258@hotmail.com.

Classifications MeSH