在体外和体内，在LPS诱导的皮肤伤口愈合模型中，telocytes抑制炎症因子表达并增强细胞迁移。,Journal of Translational Medicine

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在体外和体内，在LPS诱导的皮肤伤口愈合模型中，telocytes抑制炎症因子表达并增强细胞迁移。
Journal of Translational Medicine ( IF 6.1 ) Pub Date : 2020-02-06 , DOI: 10.1186/s12967-020-02217-y
Lu Wang ₁ , Dongli Song ₂ , Chuanyuan Wei ₁ , Cheng Chen ₁ , Yanwen Yang ₁ , Xinyi Deng ₁ , Jianying Gu ₁

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背景技术细胞增殖和死亡是伤口愈合和组织修复的关键成分。telocytes（TCs）代表了一种新发现的细胞类型，可以通过与相邻细胞的细胞间通讯保护组织免受急性伤害。这项研究的目的是使用皮肤伤口愈合和脂多糖（LPS）诱导的细胞损伤的小鼠模型来评估TCs在体内和体外对皮肤伤口愈合的影响。材料/方法进行了免疫组织化学染色以评估正常和慢性伤口患者组织中TC的变化。然后，建立了背部的雄性C57BL / 6小鼠伤口模型。将小鼠随机分为三组，并根据伤口愈合速度和组织学评估伤口愈合。建立了LPS诱导的小鼠肺tel细胞细胞系（TCs）与人角质形成细胞（HaCaT），人皮肤微血管内皮细胞（HDMEC）或鼠成纤维细胞（L929）细胞共培养模型，以分析TCs对皮肤的组成型细胞。检查细胞增殖，迁移和凋亡，并检测HaCaT细胞，HDMEC和L929细胞中的活性氧（ROS）和炎性因子，以研究参与皮肤伤口TC保护的机制。结果与健康对照组相比，慢性伤口患者组织中的TCs显着增加。与LPS诱导的模型相比，在外源性TCs处理的伤口小鼠模型中，伤口愈合得到了显着改善。TCs逆转了LPS诱导的对HaCaT细胞和HDMEC的抑制作用，并降低了LPS诱导的HaCaT细胞的凋亡以及HDMEC和L929细胞的死亡率。TC逆转了LPS诱导的HDMEC和L929细胞中的ROS，并降低了HaCaT细胞，HDMEC和L929细胞中炎症因子的mRNA水平。结论TCs减少了伤口的愈合延迟，LPS引起的炎症反应可能是由炎症抑制介导的，从而限制了细胞凋亡并促进了皮肤中主要成分细胞的迁移。

"点击查看英文标题和摘要"

Telocytes inhibited inflammatory factor expression and enhanced cell migration in LPS-induced skin wound healing models in vitro and in vivo.

BACKGROUND Cell proliferation and death are key components of wound healing and tissue repair. Telocytes (TCs) represent a newly discovered cell type that can protect tissue from acute injury via cell-cell communication with adjacent cells. The aim of this study was to use a mouse model of skin wound healing and lipopolysaccharide (LPS)-induced cell injury to evaluate the effects of TCs on skin wound healing in vivo and in vitro. MATERIAL/METHODS Immunohistochemical staining was performed to evaluate the alteration of TCs in tissues from normal and chronic wound patients. Then, a male C57BL/6 mouse wound model of the back was established. The mice were divided randomly into three groups, and wound healing was estimated according to the wound healing rate and histology. An LPS-induced co-culture model of a mouse lung telocyte cell line (TCs) with human keratinocyte (HaCaT), human dermal microvascular endothelial cell (HDMEC) or murine fibroblast (L929) cell lines was established to analyse the effects of TCs on constitutive cell types of the skin. Cell proliferation, migration and apoptosis were examined, and reactive oxygen species (ROS) and inflammatory factors in HaCaT cells, HDMECs, and L929 cells were detected to study the mechanisms involved in TC protection in skin wounds. RESULTS TCs were significantly increased in tissues from chronic wound patients compared with healthy controls. Wound healing was significantly improved in wound mouse models treated with exogenous TCs compared with LPS-induced models. TCs reversed the LPS-induced inhibition of HaCaT cells and HDMECs and reduced the LPS-induced apoptosis of HaCaT cells and the death ratios of HDMECs and L929 cells. TCs reversed LPS-induced ROS in HDMECs and L929 cells and decreased inflammatory factor mRNA levels in HaCaT cells, HDMECs and L929 cells. CONCLUSIONS TCs reduce wound healing delay, and inflammatory responses caused by LPS might be mediated by inflammatory inhibition, thus restricting apoptosis and promoting migration of the main component cell types in the skin.

更新日期：2020-02-07

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