角质形成细胞
哈卡特
伤口愈合
基因敲除
细胞迁移
细胞生物学
小RNA
表皮(动物学)
生物
转基因
转基因小鼠
细胞生长
癌症研究
免疫学
细胞
细胞培养
解剖
基因
遗传学
作者
Yan Wu,Julia Li Zhong,Ning Hou,Yaolan Sun,Benting Ma,Muhammad Nisar,Yan Teng,Zhao-Li Tan,Keping Chen,Youliang Wang,Xiao Yang
摘要
Abstract Wound healing is a complex process which involves proliferation and migration of keratinocyte for closure of epidermal injuries. A member of micro RNA family, let‐7b, has been expressed in mammalian skin, but its exact role in keratinocyte migration is still not in knowledge. Here, we showed that let‐7b regulates keratinocyte migration by targeting the insulin‐like growth factor IGF 2 BP 2. Overexpression of let‐7b led to reduced HaCaT cell migration, while knockdown of let‐7b resulted in enhanced migration. Furthermore, let‐7b was decreased during wound healing in wild‐type mice, which led us to construct the transgenic mice with overexpression of let‐7b in skin. The re‐epithelialization of epidermis of let‐7b transgenic mice was reduced during wound healing. Using bioinformatics prediction software and a reporter gene assay, we found that IGF 2 BP 2 was a target of let‐7b, which contributes to keratinocyte migration. Introduction of an expression vector of IGF 2 BP 2 also rescued let‐7b‐induced migration deficiency, which confirms that IGF 2 BP 2 is an important target for let‐7b regulation. Our findings suggest that let‐7b significantly delayed the re‐epithelialization possibly due to reduction of keratinocyte migration and restraints IGF 2 BP 2 during skin wound healing.
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