Open Access

TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14‑NF‑κB signaling pathway

  • Authors:
    • Zulong Sheng
    • Chenwei Ju
    • Bing Li
    • Zhongpu Chen
    • Xiaodong Pan
    • Gaoliang Yan
    • Yanru He
    • Yuyu Yao
    • Genshan Ma
  • View Affiliations

  • Published online on: September 6, 2018     https://doi.org/10.3892/etm.2018.6703
  • Pages: 4019-4029
  • Copyright: © Sheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute myocardial infarction (AMI) remains one of the leading causes of mortality worldwide; however, endothelial progenitor cell (EPC) transplantation has been proposed as a promising treatment strategy for EPC. High levels of tumor necrosis factor‑related weak inducer of apoptosis (TWEAK) have been reported in AMI, although its effect on EPCs has not been reported. In the present study, immunofluorescence and flow cytometry were performed to assess the effect of TWEAK in isolated mouse EPCs. Echocardiography was used to evaluate the cardiac function of murine hearts following EPC treatment in the AMI model, while collagen synthesis within the heart tissue was assessed using Masson's trichrome staining. A tube formation assay and Transwell migration assay were performed to investigate the effects of TWEAK on vessel formation and EPC migration in vitro. Angiogenesis and arteriogenesis were assessed in vivo using immunohistochemistry and western blotting was performed to determine the effect of TWEAK‑mediated nuclear factor (NF)‑κB pathway activation in EPCs. The results revealed that TWEAK promotes EPC migration, tube formation and viability in vitro. Furthermore, TWEAK treatment resulted in improved cardiac function, decreased heart collagen and vasculogenesis in mice with AMI, which was mediated by the TWEAK‑ fibroblast growth factor‑inducible 14 (Fn14)‑NF‑κB signaling pathway, as determined using Fn14 small interfering (si)RNA and Bay 11‑7082 (an NF‑κB inhibitor). In summary, the results of the present study suggest that activation of the TWEAK‑Fn14‑NF‑κB signaling pathway exerts a beneficial effect on EPCs for the treatment of AMI.
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November-2018
Volume 16 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Sheng Z, Ju C, Li B, Chen Z, Pan X, Yan G, He Y, Yao Y and Ma G: TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14‑NF‑κB signaling pathway. Exp Ther Med 16: 4019-4029, 2018
APA
Sheng, Z., Ju, C., Li, B., Chen, Z., Pan, X., Yan, G. ... Ma, G. (2018). TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14‑NF‑κB signaling pathway. Experimental and Therapeutic Medicine, 16, 4019-4029. https://doi.org/10.3892/etm.2018.6703
MLA
Sheng, Z., Ju, C., Li, B., Chen, Z., Pan, X., Yan, G., He, Y., Yao, Y., Ma, G."TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14‑NF‑κB signaling pathway". Experimental and Therapeutic Medicine 16.5 (2018): 4019-4029.
Chicago
Sheng, Z., Ju, C., Li, B., Chen, Z., Pan, X., Yan, G., He, Y., Yao, Y., Ma, G."TWEAK promotes endothelial progenitor cell vasculogenesis to alleviate acute myocardial infarction via the Fn14‑NF‑κB signaling pathway". Experimental and Therapeutic Medicine 16, no. 5 (2018): 4019-4029. https://doi.org/10.3892/etm.2018.6703