Open AccessCalcium silicate accelerates cutaneous wound healing with enhanced re-epithelialization through EGF/EGFR/ERK-mediated promotion of epidermal stem cell functions
Author(s) -
Bingmin Li,
Huadong Tang,
Xiaowei Bian,
Kui Ma,
Jiang Chang,
Xiaobing Fu,
Cuiping Zhang
Publication year - 2021
Publication title -
burns and trauma
Language(s) - English
Resource type - Journals
ISSN - 2321-3876
DOI - 10.1093/burnst/tkab029
Subject(s) - mapk/erk pathway , wound healing , microbiology and biotechnology , epidermal growth factor , cell growth , epidermal growth factor receptor , cancer research , chemistry , signal transduction , biology , immunology , receptor , biochemistry
Background Human epidermal stem cells (hESCs) play an important role in re-epithelialization and thereby in facilitating wound healing, while an effective way to activate hESCs remains to be explored. Calcium silicate (CS) is a form of bioceramic that can alter cell behavior and promote tissue regeneration. Here, we have observed the effect of CS on hESCs and investigated its possible mechanism. Methods Using a mouse full-thickness skin excision model, we explored the therapeutic effect of CS on wound healing and re-epithelialization. In vitro , hESCs were cultured with diluted CS ion extracts (CSIEs), and the proliferation, migration ability and stemness of hESCs were evaluated. The effects of CS on the epidermal growth factor (EGF), epidermal growth factor receptor (EGFR) and extracellular signal-related kinase (ERK) signaling pathway were also explored. Results In vivo , CS accelerated wound healing and re-epithelialization. Immunohistochemistry demonstrated that CS upregulated cytokeratin 19 and integrin β1 expression, indicating that CS improved hESCs stemness. In vitro studies confirmed that CS improved the biological function of hESCs. And the possible mechanism could be due to the activation of the EGF/EGFR/ERK signaling pathway. Conclusion CS can promote re-epithelialization and improve the biological functions of hESCs via activating the EGF/EGFR/ERK signaling pathway.