Open Access

Dendritic cell‑derived exosomal miR‑494‑3p promotes angiogenesis following myocardial infarction

Corrigendum in: /10.3892/ijmm.2022.5096

  • Authors:
    • Haibo Liu
    • Youming Zhang
    • Jie Yuan
    • Wei Gao
    • Xin Zhong
    • Kang Yao
    • Li Lin
    • Junbo Ge
  • View Affiliations

  • Published online on: November 2, 2020     https://doi.org/10.3892/ijmm.2020.4776
  • Pages: 315-325
  • Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Infiltration by dendritic cells (DCs) is markedly increased in the infarcted area following myocardial infarction (MI), and DC ablation has been shown to impair angiogenesis in mice post‑MI. Exosomes (EXs) have long been known to act as messengers between cells; however, whether EXs derived from DCs can enhance myocardial angiogenesis post‑MI remains unknown. The aim of the present study was to elucidate whether EXs derived from DCs induce myocardial angiogenesis via paracrine signaling post‑MI. In vitro, suspensions of mouse bone marrow‑derived DCs (BMDCs) were incubated with the supernatant of necrotic or normal cultured HL‑1 myocardial cells (as the MI or control group, respectively) for 24 h. EXs isolated from the supernatant of BMDCs were termed DEXs, which were added to primary cultures of rat cardiac microvascular endothelial cells (CMECs), and angiogenesis was evaluated by measuring tube formation and vascular endothelial growth factor (VEGF) expression. In vivo, different groups of DEXs were injected into the infarcted myocardium of MI model mice. Then, angiogenesis was evaluated by measuring the number of vessels and the expression of VEGF and CD31 in the infarcted myocardium using immunohistochemistry. Moreover, the expression profile of microRNAs (miRNAs or miRs) in splenic DCs of MI model mice was analyzed by Affymetrix miRNA 4.0 chip assays, then certified in DEXs by reverse transcription‑quantitative PCR analysis. Finally, miRNA‑loaded DEXs were used to induce tube formation by CMECs and angiogenesis in MI model mice. It was observed that, compared with the control group, DEXs from the MI group significantly upregulated the expression of VEGF in CMECs, enhanced tube formation by CMECs, and upregulated the expression of VEGF and CD31 in the infarcted myocardium of MI model mice. miR‑494‑3p and miR‑16a‑5p, which are associated with angiogenesis, were significantly upregulated in splenic DCs of MI model mice by Affymetrix miRNA 4.0 chip assays, miR‑494‑3p was significantly upregulated and highly enriched in DEXs from the MI group compared with the control, and DEX‑miR‑494‑3p enhanced tube formation by CMECs and angiogenesis in mice post‑MI. These results suggest that miR‑494‑3p may be secreted from DCs via EXs and promotes angiogenesis post‑MI. These findings indicate a novel DEX‑based approach to the treatment of MI.
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January-2021
Volume 47 Issue 1

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Spandidos Publications style
Liu H, Zhang Y, Yuan J, Gao W, Zhong X, Yao K, Lin L and Ge J: Dendritic cell‑derived exosomal miR‑494‑3p promotes angiogenesis following myocardial infarction Corrigendum in /10.3892/ijmm.2022.5096. Int J Mol Med 47: 315-325, 2021.
APA
Liu, H., Zhang, Y., Yuan, J., Gao, W., Zhong, X., Yao, K. ... Ge, J. (2021). Dendritic cell‑derived exosomal miR‑494‑3p promotes angiogenesis following myocardial infarction Corrigendum in /10.3892/ijmm.2022.5096. International Journal of Molecular Medicine, 47, 315-325. https://doi.org/10.3892/ijmm.2020.4776
MLA
Liu, H., Zhang, Y., Yuan, J., Gao, W., Zhong, X., Yao, K., Lin, L., Ge, J."Dendritic cell‑derived exosomal miR‑494‑3p promotes angiogenesis following myocardial infarction Corrigendum in /10.3892/ijmm.2022.5096". International Journal of Molecular Medicine 47.1 (2021): 315-325.
Chicago
Liu, H., Zhang, Y., Yuan, J., Gao, W., Zhong, X., Yao, K., Lin, L., Ge, J."Dendritic cell‑derived exosomal miR‑494‑3p promotes angiogenesis following myocardial infarction Corrigendum in /10.3892/ijmm.2022.5096". International Journal of Molecular Medicine 47, no. 1 (2021): 315-325. https://doi.org/10.3892/ijmm.2020.4776