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Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells

  • Authors:
    • Jingjing Chen
    • Shunen Xu
    • Wei Li
    • Lirong Wu
    • Long Wang
    • Yongkang Li
    • Wei Zhou
  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China, Department of Orthopedics, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4631-4636
    |
    Published online on: October 25, 2019
       https://doi.org/10.3892/etm.2019.8134
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Abstract

Homeobox protein Nxk‑2.5 (Nkx2.5) is a homeobox transcription factor that promotes chamber‑like myocardial gene expression. Data from a previous genome‑wide association study suggested that Nkx2.5 may be associated with the genetic variation that underlies atrial fibrillation (AF). Nkx2.5 loss of function has been demonstrated to be associated with an increasing susceptibility of familial AF. Therefore, the aim of the present study was to investigate the effect of Nkx2.5 loss of function on electrophysiological substrates in HL‑1 cells. To the best of our knowledge, the results demonstrated for the first time that Nkx2.5 expression was significantly decreased in a rat model exhibiting AF. The effect of silencing Nkx2.5 was assessed following transfection with adenoviral vectors with specific NKX2.5‑shRNA. The effect of Nkx2.5 silencing on potassium/sodium hyperpolarization‑activated cyclic nucleotide‑gated channel 4 (HCN4), gap junction alpha‑5 protein (Cx40), calcium handling proteins and protein Wnt‑11 (Wnt11) expression levels was also assessed in HL‑1 cells. The results revealed that Nkx2.5 silencing increased HCN4 expression, decreased Cx40 expression and disrupted the expression of calcium handling proteins. Additionally, Wnt11 signal protein expression was decreased following Nkx2.5 silencing. The results of the present study demonstrated that Nkx2.5 served as a transcriptional regulator of the electrophysiological substrates associated with AF.
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Copy and paste a formatted citation
Spandidos Publications style
Chen J, Xu S, Li W, Wu L, Wang L, Li Y and Zhou W: Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells. Exp Ther Med 18: 4631-4636, 2019.
APA
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., & Zhou, W. (2019). Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells. Experimental and Therapeutic Medicine, 18, 4631-4636. https://doi.org/10.3892/etm.2019.8134
MLA
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., Zhou, W."Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells". Experimental and Therapeutic Medicine 18.6 (2019): 4631-4636.
Chicago
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., Zhou, W."Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells". Experimental and Therapeutic Medicine 18, no. 6 (2019): 4631-4636. https://doi.org/10.3892/etm.2019.8134
Copy and paste a formatted citation
x
Spandidos Publications style
Chen J, Xu S, Li W, Wu L, Wang L, Li Y and Zhou W: Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells. Exp Ther Med 18: 4631-4636, 2019.
APA
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., & Zhou, W. (2019). Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells. Experimental and Therapeutic Medicine, 18, 4631-4636. https://doi.org/10.3892/etm.2019.8134
MLA
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., Zhou, W."Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells". Experimental and Therapeutic Medicine 18.6 (2019): 4631-4636.
Chicago
Chen, J., Xu, S., Li, W., Wu, L., Wang, L., Li, Y., Zhou, W."Nkx2.5 insufficiency leads to atrial electrical remodeling through Wnt signaling in HL‑1 cells". Experimental and Therapeutic Medicine 18, no. 6 (2019): 4631-4636. https://doi.org/10.3892/etm.2019.8134
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