PMID- 38237222
OWN - NLM
STAT- MEDLINE
DCOM- 20240208
LR  - 20240208
IS  - 1878-1705 (Electronic)
IS  - 1567-5769 (Linking)
VI  - 128
DP  - 2024 Feb 15
TI  - Long noncoding RNA MCM3AP-AS1 attenuates sepsis-induced cardiomyopathy by 
      improving inflammation, oxidative stress, and mitochondrial function through 
      mediating the miR-501-3p/CADM1/STAT3 axis.
PG  - 111500
LID - S1567-5769(24)00018-3 [pii]
LID - 10.1016/j.intimp.2024.111500 [doi]
AB  - Oxidative stress and inflammation are highly important for sepsis-mediated 
      myocardial damage. The long noncoding RNA (lncRNA) MCM3AP-AS1 is involved in 
      inflammatory diseases, but its function in acute myocardial injury during sepsis 
      has not been fully elucidated. LPS and cecal ligation and puncture (CLP) were 
      used to construct in vitro and in vivo sepsis-induced myocardial damage models, 
      respectively. qRT-PCR was used to evaluate alterations in MCM3AP-AS1 and 
      miR-501-3p alterations. After the MCM3AP-AS1 and miR-501-3p knockdown or 
      overexpression models were established, the viability, apoptosis, inflammation, 
      oxidative stress, and mitochondrial function of the myocardial cells were 
      examined. Dual luciferase activity assay, RNA immunoprecipitation, and 
      fluorescence in situ hybridization (FISH) confirmed the correlation among 
      MCM3AP-AS1, miR-501-3p, and CADM1. Previous studies revealed that MCM3AP-AS1 was 
      downregulated in sepsis patients, myocardial cells treated with LPS, and in the 
      CLP mouse sepsis model, whereas miR-501-3p expression was increased. MCM3AP-AS1 
      overexpression hampered myocardial damage mediated by LPS and abated 
      inflammation, oxidative stress, and mitochondrial dysfunction in myocardial cells 
      and THP-1 cells. In contrast, MCM3AP-AS1 knockdown or miR-501-3p overexpression 
      promoted all the effects of LPS. In vivo, MCM3AP-AS1 overexpression increased the 
      survival rate of CLP mice; ameliorated myocardial injury; decreased the levels of 
      TNF-alpha, IL-1beta, IL-6, iNOS, COX2, ICAM1, VCAM1, PGE2, and MDA; and increased the 
      levels of SOD, GSH-PX, Nrf2, and HO-1. Mechanistic studies demonstrated that 
      MCM3AP-AS1 acted as a competitive endogenous RNA to repress miR-501-3p, enhance 
      CADM1 expression, and dampen STAT3/nuclear factor-kappaB (NF-kappaB) activation. 
      MCM3AP-AS1 suppresses myocardial injury elicited by sepsis by mediating the 
      miR-501-3p/CADM1/STAT3/NF-kappaB axis.
CI  - Copyright (c) 2024 Elsevier B.V. All rights reserved.
FAU - Nie, Xiangbi
AU  - Nie X
AD  - Department of Emergency, Jiangxi Provincial People's Hospital, The First 
      Affiliated Hospital of Nanchang Medical College, NanChang 330006, Jiangxi, China.
FAU - Deng, Wu
AU  - Deng W
AD  - Department of Emergency, Jiangxi Provincial People's Hospital, The First 
      Affiliated Hospital of Nanchang Medical College, NanChang 330006, Jiangxi, China.
FAU - Zhou, Han
AU  - Zhou H
AD  - Department of Emergency, Jiangxi Provincial People's Hospital, The First 
      Affiliated Hospital of Nanchang Medical College, NanChang 330006, Jiangxi, China.
FAU - Wang, Zenggeng
AU  - Wang Z
AD  - Department of Emergency, Jiangxi Provincial People's Hospital, The First 
      Affiliated Hospital of Nanchang Medical College, NanChang 330006, Jiangxi, China. 
      Electronic address: wang_zenggeng@163.com.
LA  - eng
PT  - Journal Article
DEP - 20240118
PL  - Netherlands
TA  - Int Immunopharmacol
JT  - International immunopharmacology
JID - 100965259
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (NF-kappa B)
RN  - 0 (Lipopolysaccharides)
RN  - EC 2.3.1.- (MCM3AP protein, human)
RN  - EC 2.3.1.- (Acetyltransferases)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (CADM1 protein, human)
RN  - 0 (Cell Adhesion Molecule-1)
RN  - 0 (STAT3 protein, human)
RN  - 0 (MIRN501 microRNA, human)
RN  - 0 (STAT3 Transcription Factor)
SB  - IM
MH  - Humans
MH  - Animals
MH  - Mice
MH  - *MicroRNAs/genetics
MH  - *RNA, Long Noncoding/genetics
MH  - NF-kappa B/metabolism
MH  - Lipopolysaccharides/metabolism
MH  - In Situ Hybridization, Fluorescence
MH  - Inflammation
MH  - *Cardiomyopathies
MH  - Apoptosis
MH  - *Sepsis
MH  - Oxidative Stress
MH  - Acetyltransferases/genetics
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Cell Adhesion Molecule-1/genetics/metabolism
MH  - *STAT3 Transcription Factor
OTO - NOTNLM
OT  - Heart Injuries
OT  - Inflammation
OT  - Oxidative stress
OT  - Sepsis
OT  - lncRNA MCM3AP-AS1
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2024/01/19 00:42
MHDA- 2024/02/08 06:43
CRDT- 2024/01/18 18:01
PHST- 2023/03/09 00:00 [received]
PHST- 2023/12/17 00:00 [revised]
PHST- 2024/01/03 00:00 [accepted]
PHST- 2024/02/08 06:43 [medline]
PHST- 2024/01/19 00:42 [pubmed]
PHST- 2024/01/18 18:01 [entrez]
AID - S1567-5769(24)00018-3 [pii]
AID - 10.1016/j.intimp.2024.111500 [doi]
PST - ppublish
SO  - Int Immunopharmacol. 2024 Feb 15;128:111500. doi: 10.1016/j.intimp.2024.111500. 
      Epub 2024 Jan 18.