Open Access

ERK1/2 pathway regulates coxsackie and adenovirus receptor expression in mouse cardiac stem cells

  • Authors:
    • Jingjin Liu
    • Qiang Sun
    • Yongshun Wang
    • Jinjin Cui
    • Maomao Zhang
    • Lili Li
    • Haibo Jia
    • Lulu Zhang
    • Bin Zhu
    • Miaomiao Jiang
    • Bo Yu
    • Shuo Zhang
  • View Affiliations

  • Published online on: May 2, 2017     https://doi.org/10.3892/etm.2017.4414
  • Pages: 3348-3354
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Cardiac stem cells (CSCs) are the most promising and effective candidates for the therapy of cardiac regenerative diseases; however, they have marked limitations. For instance, the implantation of CSCs is hampered by factors such as their sustainability and long‑term durability. Gene modification appears to be the most effective method of optimizing CSCs and gene therapy trials have demonstrated that efficient gene transfer is key to achieving therapeutic efficacy. However, the transduction ability of adenovirus (Ad) is limited. Previous studies have reported that low expression of coxsackie and adenovirus receptor (CAR) in target cells decreases the transduction efficiency. A promising method for improving Ad‑mediated gene transfer is to increase CAR expression in target cells. The present study investigated the effect of the Raf‑mitogen‑associated protein kinase (MAPK) kinase (MEK)‑extracellular signal‑associated protein kinase (ERK) signaling pathway on the expression of CAR on CSCs, as this pathway decreases cell‑cell adhesion via cell surface molecules. The results demonstrated that interference with the Raf‑MEK‑ERK signaling pathway by knockdown of ERK1/2 upregulated the expression of CAR. The entry of the Ad into the cells was increased following inhibition of ERK1/2. Moreover, following knockdown of CAR, the entry of Ad into cells was decreased. However, knockdown of c‑Jun N‑terminal kinase and p38 as other components of the MAPK pathway did not affect CAR expression. Therefore, CAR expression in CSCs may be mediated via the Raf‑MEK‑ERK signaling pathway. Upregulation of CAR by knockdown of ERK1/2 may significantly improve Ad‑mediated genetic modification of CSCs in the treatment of cardiovascular diseases.

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June-2017
Volume 13 Issue 6

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

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Spandidos Publications style
Liu J, Sun Q, Wang Y, Cui J, Zhang M, Li L, Jia H, Zhang L, Zhu B, Jiang M, Jiang M, et al: ERK1/2 pathway regulates coxsackie and adenovirus receptor expression in mouse cardiac stem cells. Exp Ther Med 13: 3348-3354, 2017
APA
Liu, J., Sun, Q., Wang, Y., Cui, J., Zhang, M., Li, L. ... Zhang, S. (2017). ERK1/2 pathway regulates coxsackie and adenovirus receptor expression in mouse cardiac stem cells. Experimental and Therapeutic Medicine, 13, 3348-3354. https://doi.org/10.3892/etm.2017.4414
MLA
Liu, J., Sun, Q., Wang, Y., Cui, J., Zhang, M., Li, L., Jia, H., Zhang, L., Zhu, B., Jiang, M., Yu, B., Zhang, S."ERK1/2 pathway regulates coxsackie and adenovirus receptor expression in mouse cardiac stem cells". Experimental and Therapeutic Medicine 13.6 (2017): 3348-3354.
Chicago
Liu, J., Sun, Q., Wang, Y., Cui, J., Zhang, M., Li, L., Jia, H., Zhang, L., Zhu, B., Jiang, M., Yu, B., Zhang, S."ERK1/2 pathway regulates coxsackie and adenovirus receptor expression in mouse cardiac stem cells". Experimental and Therapeutic Medicine 13, no. 6 (2017): 3348-3354. https://doi.org/10.3892/etm.2017.4414