[Corrigendum] Nicorandil protects mesenchymal stem cells against hypoxia and serum deprivation-induced apoptosis

• Authors:
  • Fengyun Zhang
  • Jinjin Cui
  • Bo Lv
  • Bo Yu

• View Affiliations

  
  Affiliations: Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, P.R. China
• Published online on: September 28, 2020     https://doi.org/10.3892/ijmm.2020.4740
• Pages: 2280-2281

• Copyright : © Zhang 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 36: [Related article:] 415-423, 2015; DOI: 10.3892/ijmm.2015.2229

After the publication of the above article, the authors have realized that Figs. 2 and 4 in their paper were published with incorrect images; regarding Fig. 2, the data featured in Fig. 2A (for the H/SD + Nico 1000 μM panel) were repeated with those featured in Fig. 1C (the 6 h H/SD panel), and the data shown for Bcl-2 in Fig. 4C were selected incorrectly. These errors arose inadvertently as a consequence of misassembling the figures.

Figure 2 Nicorandil protects MSCs against H/SD-induced apoptosis. Cells were pre-incubated with nicorandil (10-1,000 μM) for 1 h in complete medium prior to exposure to H/SD. Apoptosis was reduced by nicorandil in a dose-dependent manner, as assessed using (A and B) flow cytometry and (C and D) western blot analysis. Data are presented as the mean ± SD of 3 separate experiments. *P<0.05, compared with the normal group; ▲P<0.05, compared with the H/SD control group. MSCs, mesenchymal stem cells; H/SD, hypoxia/serum deprivation; Nico, nicorandil; Cl.caspase-3, cleaved caspase-3.

Figure 4 Nicorandil exerts anti-apoptotic effects by stabilizing MMP. Western blot analysis revealed that nicorandil induced a significant increase in (C and D) the expression of anti-apoptotic Bcl-2, with a concomitant decrease in (A-D) the pro-apoptotic proteins Bax and cytochrome c, as well as apoptosis-related (E and F) capsase-3, and these effects were reversed by LY294002 [an inhibitor of phosphoinositide 3-kinase (PI3K)]. (G) Nicorandil exerted a significant inhibitory effect on mitochondrial dysfunction, as verified by JC-1 staining. Data are presented as the means ± SD of 3 separate experiments. *P<0.05, compared with the normal group; ▲P<0.05, compared with the 100 μM nicorandil-treated group. H/SD, hypoxia/serum deprivation; Nico, nicorandil; MMP, mitochondrial membrane potential; mito.cytC, mitochondrial cytochrome c; cyto.cytC, cytosolic cytochrome c; Cl.caspase-3, cleaved caspase-3.

The revised versions of Figs. 2 and 4, featuring the corrected data panels for the above-mentioned experiments, are shown on the next page. Note that the revised data shown for these Figures do not affect the overall conclusions reported in the paper. The authors express their gratitude to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused.