Mechanism of cold exposure delaying wound healing in mice

Cold temperatures have been shown to slow skin wound healing. However, the specific mechanisms underlying cold-induced impairment of wound healing remain unclear. Here, we demonstrate that small extracellular vesicles derived from cold-exposed mouse plasma (CT-sEVs) decelerate re-epithelialization, increase scar width, and weaken angiogenesis. CT-sEVs are enriched with miRNAs involved in the regulation of wound healing-related biological processes. Functional assays revealed that miR-423-3p, enriched in CT-sEVs, acts as a critical mediator in cold-induced impairment of angiogenic responses and poor wound healing by inhibiting phosphatase and poly(A) binding protein cytoplasmic 1 (PABPC1). These findings indicate that cold delays wound healing via miR-423-3p in plasma-derived sEVs through the inhibition of the ERK or AKT phosphorylation pathways. Our results enhance understanding of the molecular mechanisms by which cold exposure delays soft tissue wound healing.

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Publication Details

Journal
Journal of Nanobiotechnology
Published
2024-11-20
DOI
https://doi.org/10.1186/s12951-024-03009-y
Citations
8
Primary Topic
Extracellular vesicles in disease
Type
article
Field-Weighted Citation Impact
1.87

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article

Mechanism of cold exposure delaying wound healing in mice

Su‐Kang Shan, Yun-Yun Wu, Si-Yang He, Fu‐Xing‐Zi Li et al.
8 citations
Journal of Nanobiotechnology
Extracellular vesicles in disease
1.87
article

Mechanism of cold exposure delaying wound healing in mice

Su‐Kang Shan, Yun-Yun Wu, Si-Yang He, Fu‐Xing‐Zi Li, Jia-Yue Duan, Ye-Hui Li, Changchun Li, Ye-Chi Cao, Ke-Xin Tang, Li-Min Lei, Xiao Lin, Bei Guo, Xi Chen, Feng Xu, Yanlin Wu, Feng Wu, Rongrong Cui, Ming-Hui Zheng, Ling‐Qing Yuan, Jun-Jie Liu
article en
8 citations

Abstract

Cold temperatures have been shown to slow skin wound healing. However, the specific mechanisms underlying cold-induced impairment of wound healing remain unclear. Here, we demonstrate that small extracellular vesicles derived from cold-exposed mouse plasma (CT-sEVs) decelerate re-epithelialization, increase scar width, and weaken angiogenesis. CT-sEVs are enriched with miRNAs involved in the regulation of wound healing-related biological processes. Functional assays revealed that miR-423-3p, enriched in CT-sEVs, acts as a critical mediator in cold-induced impairment of angiogenic responses and poor wound healing by inhibiting phosphatase and poly(A) binding protein cytoplasmic 1 (PABPC1). These findings indicate that cold delays wound healing via miR-423-3p in plasma-derived sEVs through the inhibition of the ERK or AKT phosphorylation pathways. Our results enhance understanding of the molecular mechanisms by which cold exposure delays soft tissue wound healing.

Journal of NanobiotechnologyVol. 22(1)
Central South University (CN), Hunan University of Traditional Chinese Medicine (CN), Second Xiangya Hospital of Central South University (CN), Xiangya Hospital Central South University (CN)
National Natural Science Foundation of China, Central South University, Natural Science Foundation of Hainan Province, Xiangya Hospital, Central South University
Zero hunger
Openalex Percentile: Top 14%
Extracellular vesicles in disease
1.87
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