Correction: A frog peptide provides new strategies for the intervention against skin wound healing

Correction: Cellular & Molecular Biology Letters (2023) 28:61

10.1186/s11658-023-00468-3

In this article [1], the wrong figure appeared as Figs. 1, 3 and 5, S3, S5, S8, and S14; the correct figures should have appeared as shown below.

Correct Figure 1:

Fig. 1.

OA-RD17 inhibited inflammation, promoted re-epithelialization and granulation regeneration, and accelerated full-thickness wound healing in mice. A Representative images of full-thickness wound healing in mice after local application of PBS, rh-bFGF (100 ng/mL), OA-RD17 (1 nM), or scrambled peptide (1 nM) on postoperative days 0, 2, 4, 6, and 8. B Quantification of OA-RD17 on full-thickness wound regeneration in mice on postoperative days 2, 4, 6, and 8. C Representative H&E staining of wound tissue in mice on postoperative days 4 and 8. Yellow dotted lines represent areas of neoepithelium; Es: eschar; NE: neoepithelium; GT: regenerated granulation tissue; Yellow arrows represent quantified areas of regenerated granulation tissue; scale bar 200 μm. D, E Quantification of neo-epidermal and regranulation tissue thickness on postoperative days 4 and 8. F Representative images of immunohistochemical staining of epidermal cell proliferation factor Ki67 expression in epidermal region of wound tissues on postoperative day 8; red arrows indicate positive staining, scale bar 50 μm. G Quantitative expression of epidermal cell proliferation factor Ki67; positive expression is defined as intensity of positive staining per unit area. H Representative immunohistochemical images of inflammatory factors IL-6, TNF-α, and IL-1β in wound area of mice on postoperative day 8; red arrows indicate positive staining, scale bar 50 μm. I-K Quantification of IL-6, TNF-α, and IL-1β expression in wound area on day 8 after treatment; positive expression is defined as intensity of positive staining per unit area. All data are expressed as mean ± SEM from three independent experimentsperformed in quintuplicate; ns, no significance; **P < 0.01, ***P < 0.001, and ****P < 0.0001 indicate statistically significant difference compared to vehicle

Correct Figure 3:

Fig. 3.

OA-RD17 significantly decreased inflammation and promoted epidermal regeneration in diabetic patient ex vivo skin wounds. A Illustration of diabetic patient ex vivo skin wound model. B Representativeimages of H&E staining of diabetic patient ex vivo skin wound tissues on days 3 and 7. Yellow dotted lines represent areas of neoepithelium; NE: neoplastic epithelium; scale bar 200 μm. C Thickness variations in neodermis in wound tissue on days 3 and 7 of OA-RD17 treatment. D Epidermal migration length variation in neodermis in wound tissue on days 3 and 7 of OA-RD17 treatment. E Representative images of immunohistochemical staining for epidermal Ki67 expression after one week of OA-RD17 treatment; positive staining is indicated by red arrows, scale bar 50 μm. F Quantification of positive-staining intensity of Ki67 expression in epidermis. G Representative images of immunohistochemical staining for inflammatory factors IL-6, TNF-α, and IL-1β in wound area on day 7 of OA-RD17 treatment; positive staining is indicated by red arrows, scale bar 50 μm. H-J Quantification of intensity of IL-6, TNF-α, and IL-1β expression in wound area. All data are expressed as mean ± SEM from three independent experiments performed in triplicate. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 indicate statistically significant difference compared to vehicle

Correct Figure 5:

Fig. 5.

OA-RD17 suppressed inflammatory factor expression and activated the MAPK signaling pathway to promote keratinocyte proliferation and migration. A, B ELISA analysis of effects of OA-RD17 on inflammatory factors (IL-6 and TNF-α) release in keratinocytes after LPS stimulation. C Representative image of MAPK signalling pathway activation in keratinocytes after 24 h of OA-RD17 treatment, determined by western blotting. D Quantification of P38, ERK, and JNK protein phosphorylation. E–G RT-qPCR analysis of Ki67, CDK2, and CyclinA1 mRNA expression in OA-RD17-treated keratinocytes. H Changes in pro-proliferation activity of OA-RD17 in keratinocytes after application of MAPK signaling pathway inhibitors. I Representative images ofeffects of OA-RD17 on keratinocyte scratch repair after application of MAPK signaling pathway inhibitors. J Quantification of effects of OA-RD17 on keratinocyte scratch repair rate after application of MAPK signalling pathway inhibitors. All data are expressed as mean ± SEM from three independent experiments, *P 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

Correct Figure S3:

Fig. S3.

Pro-healing ability of OA-RD17 at cellular level

Correct Figure S5:

Fig. S5.

OA-RD17 promoted macrophage polarization from MI to MII phenotype

Correct Figure S8:

Fig. S8.

Polarization of macrophages in wound area of mice with deep second-degree burns on days 8 and 14

Correct Figure S14:

Fig. S14.

Inhibition of miR-632 expression significantly inhibited keratinocyte proliferation and migration, while OA-RD17 restored effect of miR-632 down-regulation on keratinocyte proliferation and migration