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Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3

  • Authors:
    • Wei Li
    • Yuanhong Li
    • Shengyu Cui
    • Jiayi Liu
    • Lijiao Tan
    • Hao Xia
    • Changjiang Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Cardiovascular Biology, The Central Hospital of Enshi Autonomous Prefecture, Enshi, Hubei 445000, P.R. China, Medical School of Enshi Polytechnic, Enshi, Hubei 445000, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 1269
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    Published online on: September 7, 2021
       https://doi.org/10.3892/etm.2021.10704
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Abstract

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 α‑smooth muscle actin (α‑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‑α, IL‑1β (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.
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Copy and paste a formatted citation
Spandidos Publications style
Li W, Li Y, Cui S, Liu J, Tan L, Xia H and Zhang C: Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3. Exp Ther Med 22: 1269, 2021.
APA
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., & Zhang, C. (2021). Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3. Experimental and Therapeutic Medicine, 22, 1269. https://doi.org/10.3892/etm.2021.10704
MLA
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., Zhang, C."Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3". Experimental and Therapeutic Medicine 22.5 (2021): 1269.
Chicago
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., Zhang, C."Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1269. https://doi.org/10.3892/etm.2021.10704
Copy and paste a formatted citation
x
Spandidos Publications style
Li W, Li Y, Cui S, Liu J, Tan L, Xia H and Zhang C: Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3. Exp Ther Med 22: 1269, 2021.
APA
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., & Zhang, C. (2021). Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3. Experimental and Therapeutic Medicine, 22, 1269. https://doi.org/10.3892/etm.2021.10704
MLA
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., Zhang, C."Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3". Experimental and Therapeutic Medicine 22.5 (2021): 1269.
Chicago
Li, W., Li, Y., Cui, S., Liu, J., Tan, L., Xia, H., Zhang, C."Se alleviates homocysteine‑induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1269. https://doi.org/10.3892/etm.2021.10704
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