PMID- 35058120
OWN - NLM
STAT- MEDLINE
DCOM- 20220405
LR  - 20220614
IS  - 1876-4738 (Electronic)
IS  - 0914-5087 (Linking)
VI  - 79
IP  - 5
DP  - 2022 May
TI  - Low-density lipoprotein receptor and apolipoprotein A 5, myocardial infarction 
      biomarkers in plasma-derived exosomes.
PG  - 605-610
LID - S0914-5087(21)00300-2 [pii]
LID - 10.1016/j.jjcc.2021.10.020 [doi]
AB  - OBJECTIVES: Myocardial infarction (MI), a leading cause of death around the 
      world, displays a complex pattern of inheritance. Previously, rare mutations in 
      low-density lipoprotein receptor (LDLR) genes and apolipoprotein A V (APOA5) have 
      been shown to contribute to MI risk in individual families. Exosomes provide a 
      potential source of biomarkers for MI. This study is to determine the role of 
      LDLR and APOA5 as biomarkers for early diagnosis of MI. METHODS: In this study, 
      we detected the levels of LDLR, APOA5, and cardiac troponin T in plasma-derived 
      exosomes in MI patients and age-matched healthy people by enzyme linked 
      immunosorbent assay and observed the morphology and number of exosomes using 
      transmission electron microscope and nanoparticle tracking analysis. 
      Oxygen-glucose deprivation (OGD) method was used to induce MI in H9C2 
      cardiomyocytes to explore the effect of exosomes. RESULTS: We found that the 
      levels of LDLR and APOA5 in plasma-derived exosomes in MI patients were 
      significantly decreased. Furthermore, exosomes of MI patients were significantly 
      larger in size and the concentration of exosomes was higher than that of 
      age-matched non-MI people. In vitro experiments showed that OGD treatment induced 
      apoptosis of myocardial cells and decreased the expression of LDLR and APOA5, 
      while addition of exosomes isolated from healthy people rescued these phenotypes. 
      CONCLUSION: Exosomal APOA5 and LDLR are intimately associated with MI, and 
      thereby have the potential to function as diagnostic markers of MI.
CI  - Copyright (c) 2021. Published by Elsevier Ltd.
FAU - He, Yue
AU  - He Y
AD  - Department of Cardiology, Shanghai Xuhui District Central Hospital, Shanghai, 
      China.
FAU - Gu, Xinsheng
AU  - Gu X
AD  - Department of Cardiology, Shanghai Xuhui District Central Hospital, Shanghai, 
      China.
FAU - Hu, Ying
AU  - Hu Y
AD  - Department of Geriatric Medicine, Shanghai Xuhui District Central Hospital, 
      Shanghai, China.
FAU - Jia, Hao
AU  - Jia H
AD  - The First Department of Medical Affairs, Affiliated Renji Hospital, Shanghai 
      JiaoTong University, Shanghai, China.
FAU - Zhao, Zhibo
AU  - Zhao Z
AD  - Department of Cardiology, Shanghai Xuhui District Central Hospital, Shanghai, 
      China.
FAU - Jiang, Haisong
AU  - Jiang H
AD  - Institute of Neurology, Sichuan Academy of Medical Sciences & Sichuan Provincial 
      People's Hospital, Chengdu, China. Electronic address: jhsarchangle@hotmail.com.
FAU - Zheng, Hongchao
AU  - Zheng H
AD  - Department of Cardiology, Shanghai Xuhui District Central Hospital, Shanghai, 
      China. Electronic address: zhenghcao@126.com.
FAU - Zhu, Fu
AU  - Zhu F
AD  - Department of Cardiology, Shanghai Xuhui District Central Hospital, Shanghai, 
      China. Electronic address: zhufu@xh.sh.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220117
PL  - Netherlands
TA  - J Cardiol
JT  - Journal of cardiology
JID - 8804703
RN  - 0 (APOA5 protein, human)
RN  - 0 (Apolipoprotein A-V)
RN  - 0 (Apolipoproteins)
RN  - 0 (Biomarkers)
RN  - 0 (Lipoproteins, LDL)
SB  - IM
MH  - *Apolipoprotein A-V/blood/genetics/metabolism
MH  - Apolipoproteins/metabolism
MH  - Biomarkers/blood/metabolism
MH  - *Exosomes/metabolism
MH  - Humans
MH  - *Lipoproteins, LDL/blood/metabolism
MH  - *Myocardial Infarction/blood/metabolism
OTO - NOTNLM
OT  - Apolipoprotein A V
OT  - Exosome
OT  - Low-density lipoprotein receptor
OT  - Myocardial infarction
OT  - Nanoparticle tracking analysis
OT  - Transmission electron microscope
COIS- Conflict of Interest Statement The authors declare that the research was 
      conducted in the absence of any commercial or financial relationships that could 
      be construed as a potential conflict of interest.
EDAT- 2022/01/22 06:00
MHDA- 2022/04/06 06:00
CRDT- 2022/01/21 05:55
PHST- 2021/04/01 00:00 [received]
PHST- 2021/09/16 00:00 [revised]
PHST- 2021/09/21 00:00 [accepted]
PHST- 2022/01/22 06:00 [pubmed]
PHST- 2022/04/06 06:00 [medline]
PHST- 2022/01/21 05:55 [entrez]
AID - S0914-5087(21)00300-2 [pii]
AID - 10.1016/j.jjcc.2021.10.020 [doi]
PST - ppublish
SO  - J Cardiol. 2022 May;79(5):605-610. doi: 10.1016/j.jjcc.2021.10.020. Epub 2022 Jan 
      17.