PMID- 34594406
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211002
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Print)
IS  - 1792-0981 (Linking)
VI  - 22
IP  - 5
DP  - 2021 Nov
TI  - Se alleviates homocysteine-induced fibrosis in cardiac fibroblasts via 
      downregulation of lncRNA MEG3.
PG  - 1269
LID - 10.3892/etm.2021.10704 [doi]
LID - 1269
AB  - Selenium (Se) is considered to have antioxidant properties, which are beneficial 
      for heart condition. Hyperhomocysteinemia (HHCY) has been suggested to 
      potentially lead to heart failure and is characterized by cardiac fibrosis; 
      however, investigation on the role of Se and HHCY in cardiac fibrosis is rare. 
      Since previous studies demonstrated the important role of the long non-coding RNA 
      maternally expressed 3 (MEG3) in some heart diseases, the present study aimed to 
      determine how Se and MEG3 might exert regulatory effects on HCY-induced fibrosis 
      in cardiac fibroblasts (CFs). Mouse CFs were isolated and treated with HCY and 
      Se. The expression of alpha-smooth muscle actin (alpha-SMA), collagen I and III was 
      detected by western blotting to reflect CF fibrosis. Reverse 
      transcription-quantitative PCR was performed to determine the expression levels 
      of MEG3. Inflammation and oxidative stress responses were analyzed by measuring 
      TNF-alpha, IL-1beta (ELISA) and reactive oxygen species levels (using a commercial kit), 
      respectively. Cell Counting Kit-8 was used to evaluate CF proliferation. Total 
      and phosphorylated (p) expression of janus kinase 2 (JAK2) and signal transducer 
      and activator of transcription 3 (STAT3) was evaluated by western blotting. CFs 
      were transfected with adenovirus expressing MEG3 short-hairpin RNA to knock down 
      MEG3 expression. Se treatment downregulated the expression level of MEG3 in 
      HCY-stimulated CFs, whilst inhibiting the inflammatory and oxidative stress 
      response. Furthermore, Se inhibited the increased proliferation of CFs following 
      HCY treatment. In addition, MEG3-knockdown in CFs could improve fibrosis caused 
      by HCY. Furthermore, the ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were decreased 
      following treatment with Se or MEG3 silencing. Taken together, the findings from 
      the present study suggested that Se may alleviate cardiac fibrosis by 
      downregulating the expression of MEG3 and reducing the inflammatory and oxidative 
      stress response in CFs. This suggests that Se may be a potential therapeutic 
      option for treating cardiac fibrosis in the future.
CI  - Copyright: (c) Li et al.
FAU - Li, Wei
AU  - Li W
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Li, Yuanhong
AU  - Li Y
AD  - Department of Cardiovascular Biology, The Central Hospital of Enshi Autonomous 
      Prefecture, Enshi, Hubei 445000, P.R. China.
FAU - Cui, Shengyu
AU  - Cui S
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Liu, Jiayi
AU  - Liu J
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Tan, Lijiao
AU  - Tan L
AD  - Medical School of Enshi Polytechnic, Enshi, Hubei 445000, P.R. China.
FAU - Xia, Hao
AU  - Xia H
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Zhang, Changjiang
AU  - Zhang C
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
AD  - Department of Cardiovascular Biology, Minda Hospital of Hubei Minzu University, 
      Enshi, Hubei 445000, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20210907
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC8456485
OTO - NOTNLM
OT  - cardiac fibroblasts
OT  - cardiac fibrosis
OT  - hyperhomocysteinemia
OT  - long non-coding RNA maternally expressed 3
OT  - selenium
COIS- The authors declare that they have no competing interests.
EDAT- 2021/10/02 06:00
MHDA- 2021/10/02 06:01
PMCR- 2021/09/07
CRDT- 2021/10/01 07:27
PHST- 2021/03/16 00:00 [received]
PHST- 2021/08/11 00:00 [accepted]
PHST- 2021/10/01 07:27 [entrez]
PHST- 2021/10/02 06:00 [pubmed]
PHST- 2021/10/02 06:01 [medline]
PHST- 2021/09/07 00:00 [pmc-release]
AID - ETM-22-5-10704 [pii]
AID - 10.3892/etm.2021.10704 [doi]
PST - ppublish
SO  - Exp Ther Med. 2021 Nov;22(5):1269. doi: 10.3892/etm.2021.10704. Epub 2021 Sep 7.