Subvacuum environment‐enhanced cell migration promotes wound healing without increasing hypertrophic scars caused by excessive cell proliferation

伤口愈合 细胞迁移 细胞生物学 细胞生长 细胞 哈卡特 PI3K/AKT/mTOR通路 皮肤修复 蛋白激酶B 化学 细胞内 增生性瘢痕 生物 免疫学 信号转导 解剖 生物化学 体外
作者
Jian Jin,Bohan Pan,Kang‐an Wang,Shaoshuo Yu,Wu Guo-sheng,Fang He,Banghui Zhu,Yu Chen,Liangliang Zhu,Yan Liu,Zhaofan Xia,Shihui Zhu,Yu Sun
出处
期刊:Cell Proliferation [Wiley]
卷期号:56 (11): e13493-e13493 被引量:15
标识
DOI:10.1111/cpr.13493
摘要

Abstract Cell migration and proliferation are conducive to wound healing; however, regulating cell proliferation remains challenging, and excessive proliferation is an important cause of scar hyperplasia. Here, we aimed to explore how a subvacuum environment promotes wound epithelisation without affecting scar hyperplasia. Human immortalized keratinocyte cells and human skin fibroblasts were cultured under subvacuum conditions (1/10 atmospheric pressure), and changes in cell proliferation and migration, target protein content, calcium influx, and cytoskeleton and membrane fluidity were observed. Mechanical calcium (Ca 2+ ) channel blockers were used to prevent Ca 2+ influx for reverse validation. A rat wound model was used to elucidate the mechanism of the subvacuum dressing in promoting healing. The subvacuum environment was observed to promote cell migration without affecting cell proliferation; intracellular Ca 2+ concentrations and PI3K, p‐PI3K, AKT1, p‐AKT 1 levels increased significantly. The cytoskeleton was depolymerized, pseudopodia were reduced or absent, and membrane fluidity increased. The use of Ca 2+ channel blockers weakened or eliminated these changes. Animal experiments confirmed these phenomena and demonstrated that subvacuum dressings can effectively promote wound epithelisation. Our study demonstrates that the use of subvacuum dressings can enhance cell migration without affecting cell proliferation, promote wound healing, and decrease the probability of scar hyperplasia.

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