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Suppression of LRRC19 promotes cutaneous wound healing in pressure ulcers in mice.
Organogenesis ( IF 1.6 ) Pub Date : 2018-02-20 , DOI: 10.1080/15476278.2018.1436924
Jie Sun 1 , Zhijing Wang 2 , Xirui Wang 1
Affiliation  

The ischemia-reperfusion (I/R) induced skin lesion has been identified as primary cause of pressure ulcer. Better understanding of the mechanism is required for new therapy development. Leucine rich repeat containing protein 19 (LRRC19) is a recently discovered transmembrane protein containing leucine-rich repeats and plays a role in immune response. To investigate the role of LRRC19 in pressure ulcers, mouse ulcer model was established with two cycles of I/R. The expression of LRRC19 was assessed during injury. siRNA mediated LRRC19 downregulation was applied to investigate the disease severity, immune cell infiltration and pro-inflammatory cytokines production. The primary skin fibroblasts were stimulated with IL-1β to dissect the molecular mechanism. LRRC19 was readily induced in I/R induced lesion site in a pattern mimicking the disease progress as measured by wound area. Knockdown of LRRC19 by siRNA significantly alleviated the disease severity and attenuated immune cell infiltration and pro-inflammatory cytokines production. In primary skin fibroblast model, siRNA knockdown of LRRC19 suppressed IL-1β mediated NFκB activation and its downstream cytokines production. LRRC19 was a novel factor for I/R-induced tissue damage by promoting NFκB dependent pro-inflammatory response. Our results supported that LRRC19 could be a potential therapeutic target for pressure ulcers.



中文翻译:

LRRC19的抑制促进小鼠压疮的皮肤伤口愈合。

缺血再灌注(I / R)引起的皮肤病变已被确定为压疮的主要原因。新疗法的开发需要更好地了解其机制。富含亮氨酸的重复序列蛋白19(LRRC19)是最近发现的含有富含亮氨酸的重复序列的跨膜蛋白,在免疫应答中起作用。为了研究LRRC19在压力性溃疡中的作用,建立了具有两个I / R周期的小鼠溃疡模型。在损伤期间评估LRRC19的表达。siRNA介导的LRRC19下调被用于研究疾病的严重程度,免疫细胞浸润和促炎细胞因子的产生。用IL-1β刺激原代皮肤成纤维细胞,分析其分子机制。LRRC19很容易在I / R诱导的病变部位被诱导,其模式类似于通过伤口面积测量的疾病进展。siRNA抑制LRRC19可以大大减轻疾病的严重程度,并减弱免疫细胞的浸润和促炎性细胞因子的产生。在原代皮肤成纤维细胞模型中,LRRC19的siRNA抑制可抑制IL-1β介导的NFκB活化及其下游细胞因子的产生。LRRC19通过促进NFκB依赖性促炎反应,成为I / R诱导的组织损伤的新因素。我们的结果支持LRRC19可能是压力性溃疡的潜在治疗靶标。LRRC19的siRNA抑制可抑制IL-1β介导的NFκB活化及其下游细胞因子的产生。LRRC19通过促进NFκB依赖性促炎反应,成为I / R诱导的组织损伤的新因素。我们的结果支持LRRC19可能是压力性溃疡的潜在治疗靶标。LRRC19的siRNA抑制可抑制IL-1β介导的NFκB活化及其下游细胞因子的产生。LRRC19通过促进NFκB依赖性促炎反应,成为I / R诱导的组织损伤的新因素。我们的结果支持LRRC19可能是压力性溃疡的潜在治疗靶标。

更新日期:2018-02-20
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