Open Access

CXCR4 protects bone marrow‑derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway

  • Authors:
    • Zheng-Yu Liu
    • Qiu-Xia Yang
    • Yan Cao
    • Hong-Wei Pan
    • Jing-Jing Rong
    • Jing Ling
    • Yi Tang
    • Jin He
    • Chang-Lu Wang
    • Xiang Peng
    • Qiong-Chao Zou
    • Le Zhang
    • Jiao Zheng
    • Jia Wang
    • Yu Zhang
    • Jian-Qiang Peng
    • Lan-Bing Xiong
    • Feng Liu
    • Zi-Hui Ying
    • Zhao-Fen Zheng
    • Bai-Ling Zhang
  • View Affiliations

  • Published online on: August 23, 2021     https://doi.org/10.3892/etm.2021.10634
  • Article Number: 1200
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].

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Abstract

The present study aimed to investigate the regulatory mechanism of chemokine (C‑X‑C motif) receptor 4 (CXCR4) on endothelial progenitor cells (EPCs) through the phosphatidylinositol 3‑kinase/protein kinase B (PI3K/Akt) signaling pathway under hypoxic conditions. Mononuclear cells were isolated from the bone marrow (BM) of young Sprague‑Dawley (SD) rats. Bone marrow‑derived endothelial progenitor cells (BM‑EPCs) were characterized by using Dil‑labeled acetylated low‑density lipoprotein (Dil‑ac‑LDL) and fluorescein isothiocyanate‑labeled UEA (FITC‑UEA‑1). Phenotype identification of BM‑EPCs was based on red cytoplasm and green cytomembrane. Flow cytometry was employed to examine the markers CD14, CD34, and KDR. Expression level of the EPC‑specific surface marker CD14 was found to be negative, while the expression level of CD34 and KDR was positive. In addition, CXCR4 was stably overexpressed in BM‑EPCs after transfection with adenovirus‑CXCR4. Cell proliferation, migration and apoptosis abilities were measured through the application of CCK‑8, followed by Transwell and flow cytometry assays. The expression level of CXCR4, PI3K and Akt was determined by reverse transcription‑quantitative PCR and western blotting assays. Functional experiments demonstrated that hypoxia inhibited BM‑EPC proliferation and migration, while accelerating BM‑EPC apoptosis. Additionally, CXCR4 was found to promote proliferation and migration, and suppress apoptosis in BM‑EPCs with or without hypoxia treatment. Evidence also demonstrated that CXCR4 markedly upregulated the expression levels of PI3K and Akt. Furthermore, PI3K inhibitor (LY294002) and CXCR4 inhibitor (AMD3100) effectively inhibited the proliferation, migration and resistance to apoptosis of CXCR4‑mediated BM‑EPCs under hypoxic conditions.
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November-2021
Volume 22 Issue 5

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

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Copy and paste a formatted citation
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Spandidos Publications style
Liu Z, Yang Q, Cao Y, Pan H, Rong J, Ling J, Tang Y, He J, Wang C, Peng X, Peng X, et al: CXCR4 protects bone marrow‑derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway. Exp Ther Med 22: 1200, 2021
APA
Liu, Z., Yang, Q., Cao, Y., Pan, H., Rong, J., Ling, J. ... Zhang, B. (2021). CXCR4 protects bone marrow‑derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway. Experimental and Therapeutic Medicine, 22, 1200. https://doi.org/10.3892/etm.2021.10634
MLA
Liu, Z., Yang, Q., Cao, Y., Pan, H., Rong, J., Ling, J., Tang, Y., He, J., Wang, C., Peng, X., Zou, Q., Zhang, L., Zheng, J., Wang, J., Zhang, Y., Peng, J., Xiong, L., Liu, F., Ying, Z., Zheng, Z., Zhang, B."CXCR4 protects bone marrow‑derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway". Experimental and Therapeutic Medicine 22.5 (2021): 1200.
Chicago
Liu, Z., Yang, Q., Cao, Y., Pan, H., Rong, J., Ling, J., Tang, Y., He, J., Wang, C., Peng, X., Zou, Q., Zhang, L., Zheng, J., Wang, J., Zhang, Y., Peng, J., Xiong, L., Liu, F., Ying, Z., Zheng, Z., Zhang, B."CXCR4 protects bone marrow‑derived endothelial progenitor cells against hypoxia through the PI3K/Akt signaling pathway". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1200. https://doi.org/10.3892/etm.2021.10634