PMID- 32880505
OWN - NLM
STAT- MEDLINE
DCOM- 20210106
LR  - 20210106
IS  - 1743-5404 (Electronic)
IS  - 1743-5390 (Linking)
VI  - 14
IP  - 9
DP  - 2020 Nov
TI  - miR-205/IRAK2 signaling pathway is associated with urban airborne PM(2.5)-induced 
      myocardial toxicity.
PG  - 1198-1212
LID - 10.1080/17435390.2020.1813824 [doi]
AB  - Exposure to fine particulate matter (PM(2.5)) is closely linked with 
      cardiovascular diseases. However, the underlying mechanism of PM(2.5) on cardiac 
      function remains unknown. This study was aimed to investigate the role of 
      microRNA-205 (miR-205) on PM(2.5)-induced myocardial inflammation and cardiac 
      dysfunction. PM(2.5) increased the levels of reactive oxygen species (ROS) and 
      malondialdehyde (MDA), following by decreased cell viability and antioxidant 
      enzymes, resulting in apoptosis of cardiomyocytes (AC16). The histopathological 
      and ultrastructural analysis demonstrated that PM(2.5) caused myocardial damage 
      via interstitial edema, inflammatory cell infiltration, and myocardial fiber 
      destruction. PM(2.5) enhanced the release of inflammatory factors in AC16 cells 
      and heart tissue. Microarray analysis and dual-luciferase reporter gene assays 
      demonstrated that PM(2.5)-induced down-regulation of miR-205 regulated 
      interleukin 1 receptor-associated kinase 2 (IRAK2), which further activated the 
      TNF receptor-associated factor 6 (TRAF6)/nuclear transcription factor-kappaB (NF-kappaB) 
      signaling pathway in vivo. Moreover, the chemical mimics of miR-205 markedly 
      inhibited the IRAK2/TRAF6/NF-kappaB signaling pathway, whereas the chemical 
      inhibitors of miR-205 amplified PM(2.5)-induced activation of the IRAK2 signaling 
      pathway in vitro. In summary, our results found that PM(2.5) could trigger 
      myocardial toxicity via miR-205 negative regulating the IRAK2/TRAF6/NF-kappaB 
      signaling pathway. Our study suggests that miR-205 could be a promising target 
      molecule for mitigating the hazardous effects of PM(2.5) on the cardiovascular 
      system.
FAU - Feng, Lin
AU  - Feng L
AD  - Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital 
      Medical University, Beijing, P.R. China.
AD  - Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, P.R. China.
FAU - Wei, Jialiu
AU  - Wei J
AD  - Key Laboratory of Cardiovascular Epidemiology & Department of Epidemiology, Fuwai 
      Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical 
      Sciences and Peking Union Medical College, Beijing, China.
FAU - Liang, Shuang
AU  - Liang S
AD  - Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital 
      Medical University, Beijing, P.R. China.
AD  - Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, P.R. China.
FAU - Sun, Zhiwei
AU  - Sun Z
AD  - Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital 
      Medical University, Beijing, P.R. China.
AD  - Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, P.R. China.
FAU - Duan, Junchao
AU  - Duan J
AD  - Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital 
      Medical University, Beijing, P.R. China.
AD  - Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, 
      Beijing, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20200903
PL  - England
TA  - Nanotoxicology
JT  - Nanotoxicology
JID - 101233132
RN  - 0 (Air Pollutants)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MIRN205 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (Particulate Matter)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tifab protein, human)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
SB  - IM
MH  - Air Pollutants/chemistry/*toxicity
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Down-Regulation/drug effects
MH  - Gene Expression Regulation/drug effects
MH  - Heart/*drug effects
MH  - Humans
MH  - Interleukin-1 Receptor-Associated Kinases/genetics/*metabolism
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Male
MH  - Malondialdehyde/metabolism
MH  - MicroRNAs/genetics/*metabolism
MH  - Myocardium/*metabolism/ultrastructure
MH  - Myocytes, Cardiac/drug effects/metabolism/ultrastructure
MH  - NF-kappa B/genetics/metabolism
MH  - Particulate Matter/chemistry/*toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species/metabolism
MH  - Signal Transduction
OTO - NOTNLM
OT  - Fine particulate matter
OT  - IRAK2/TRAF6/NF-kappaB signaling pathway
OT  - cardiac function
OT  - miR-205
OT  - myocardial toxicity
EDAT- 2020/09/04 06:00
MHDA- 2021/01/07 06:00
CRDT- 2020/09/04 06:00
PHST- 2020/09/04 06:00 [pubmed]
PHST- 2021/01/07 06:00 [medline]
PHST- 2020/09/04 06:00 [entrez]
AID - 10.1080/17435390.2020.1813824 [doi]
PST - ppublish
SO  - Nanotoxicology. 2020 Nov;14(9):1198-1212. doi: 10.1080/17435390.2020.1813824. 
      Epub 2020 Sep 3.