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

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

• View Affiliations

  
  Affiliations: Department of Cardiology, Qingpu Branch of Zhongshan Hospital, Fudan University, Shanghai 201700, P.R. China, Department of Cardiology, Shanghai East Hospital, Tongji University, Shanghai 200120, P.R. China, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China
• Published online on: February 1, 2022     https://doi.org/10.3892/ijmm.2022.5096
• Article Number: 41

• Copyright : © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

Article

Int J Mol Med 47: [Related article:] 315-325, 2021; DOI: 10.3892/ijmm.2020.4776

Following the publication of the above article, the authors have realized that they inadvertently included incorrect data panels in Fig. 7 on p. 323; specifically, while preparing the figure, the panels denoting the 'CD31 DEXs-miRNA-194-3p inhibitor' and 'VEGF-DEXs-blank' panels were imported incorrectly in Fig. 7C.

Figure 7 DEXs-miRNA-494-3p induces angiogenesis in MI model mice. (A) The expression levels of CD31 and VEGF in the infarcted myocardium of MI model mice induced by DEXs-miRNA-494-3p mimic were determined by immunohistochemistry. (B) Comparison of vessel counts in the infarcted area among different groups (n=6-7). *P<0.05 vs. DEXs blank and DEXs mimic NC. (C) The expression of CD31 and VEGF in the infarcted myocardium of MI model mice induced by DEXs-miRNA-494-3p inhibitor was determined by immunohistochemistry. (D) The mean number of CD31-positive capillaries/mm2 were counted in the infarcted area in five fields per sample under an optical microscope and compared among different groups (n=6-7). *P<0.05 vs. DEXs blank and DEXs inhibitor NC. Magnification, x400. NS, not significant; MI, myocardial infarction; DEXs, dendritic cell-derived exosomes; VEGF, vascular endothelial growth factor; miRNA, microRNA; NC, negative control.

The revised version of Fig. 7, containing the correct data for the abovementioned panels, is shown below. Note that the errors made during the assembly of this figure did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused.

Figure 7 DEXs-miRNA-494-3p induces angiogenesis in MI model mice. (A) The expression levels of CD31 and VEGF in the infarcted myocardium of MI model mice induced by DEXs-miRNA-494-3p mimic were determined by immunohistochemistry. (B) Comparison of vessel counts in the infarcted area among different groups (n=6-7). *P<0.05 vs. DEXs blank and DEXs mimic NC. (C) The expression of CD31 and VEGF in the infarcted myocardium of MI model mice induced by DEXs-miRNA-494-3p inhibitor was determined by immunohistochemistry. (D) The mean number of CD31-positive capillaries/mm2 were counted in the infarcted area in five fields per sample under an optical microscope and compared among different groups (n=6-7). *P<0.05 vs. DEXs blank and DEXs inhibitor NC. Magnification, x400. NS, not significant; MI, myocardial infarction; DEXs, dendritic cell-derived exosomes; VEGF, vascular endothelial growth factor; miRNA, microRNA; NC, negative control.