PDF(Pubmed)
Abstract：
UNASSIGNED: Atopic dermatitis (AD) is a common chronic inflammatory skin diseases that seriously affects life quality of the patients. Staphylococcus aureus (S. aureus) colonization on the skin plays an important role in the pathogenesis of AD; however, the mechanism of how it modulates skin immunity to exacerbate AD remains unclear. MicroRNAs are short non-coding RNAs that act as post-transcriptional regulators of genes. They are involved in the pathogenesis of various inflammatory skin diseases.
UNASSIGNED: In this study, we established miRNA expression profiles for keratinocytes stimulated with heat-killed S. aureus (HKSA). The expression of miR-939 in atopic dermatitis patients was analyzed by fluorescence in situ hybridization (FISH). miR-939 mimic was transfected to human primary keratinocyte to investigate its impact on the expression of matrix metalloproteinase genes (MMPs) in vitro. Subsequently, miR-939, along with Polyplus transfection reagent, was administered to MC903-induced atopic dermatitis skin to assess its function in vivo.
UNASSIGNED: MiR-939 was highly upregulated in HKSA-stimulated keratinocytes and AD lesions. In vitro studies revealed that miR-939 increased the expression of matrix metalloproteinase genes, including MMP1, MMP3, and MMP9, as well as the cell adhesion molecule ICAM1 in human primary keratinocytes. In vivo studies indicated that miR-939 increased the expression of matrix metalloproteinases to promote the colonization of S. aureus and exacerbated S. aureus-induced AD-like skin inflammation.
UNASSIGNED: Our work reveals miR-939 is an important regulator of skin inflammation in AD that could be used as a potential therapeutic target for AD.
UNASSIGNED: In this study, we established miRNA expression profiles for keratinocytes stimulated with heat-killed S. aureus (HKSA). The expression of miR-939 in atopic dermatitis patients was analyzed by fluorescence in situ hybridization (FISH). miR-939 mimic was transfected to human primary keratinocyte to investigate its impact on the expression of matrix metalloproteinase genes (MMPs) in vitro. Subsequently, miR-939, along with Polyplus transfection reagent, was administered to MC903-induced atopic dermatitis skin to assess its function in vivo.
UNASSIGNED: MiR-939 was highly upregulated in HKSA-stimulated keratinocytes and AD lesions. In vitro studies revealed that miR-939 increased the expression of matrix metalloproteinase genes, including MMP1, MMP3, and MMP9, as well as the cell adhesion molecule ICAM1 in human primary keratinocytes. In vivo studies indicated that miR-939 increased the expression of matrix metalloproteinases to promote the colonization of S. aureus and exacerbated S. aureus-induced AD-like skin inflammation.
UNASSIGNED: Our work reveals miR-939 is an important regulator of skin inflammation in AD that could be used as a potential therapeutic target for AD.
摘要：
■特应性皮炎(AD)是一种常见的慢性炎症性皮肤病,严重影响患者的生活质量。金黄色葡萄球菌（S。金黄色葡萄球菌)在皮肤上的定植在AD的发病机制中起重要作用；然而，其调节皮肤免疫以加重AD的机制尚不清楚.MicroRNA是短的非编码RNA,其充当基因的转录后调节因子。它们参与各种炎性皮肤病的发病机理。
■在这项研究中，我们建立了热灭活金黄色葡萄球菌(HKSA)刺激的角质形成细胞的miRNA表达谱.采用荧光原位杂交(FISH)分析特应性皮炎患者中miR-939的表达。将miR-939模拟物转染至人原代角质形成细胞以研究其在体外对基质金属蛋白酶基因(MMPs)表达的影响。随后，miR-939，以及Polyplus转染试剂，给予MC903诱导的特应性皮炎皮肤以评估其体内功能。
■MiR-939在HKSA刺激的角质形成细胞和AD病变中高度上调。体外研究显示miR-939增加了基质金属蛋白酶基因的表达,包括MMP1，MMP3和MMP9，以及人原代角质形成细胞中的细胞粘附分子ICAM1。体内研究表明miR-939增加基质金属蛋白酶的表达以促进金黄色葡萄球菌的定植并加剧金黄色葡萄球菌诱导的AD样皮肤炎症。
■我们的工作揭示miR-939是AD中皮肤炎症的重要调节因子，可用作AD的潜在治疗靶点。
■在这项研究中，我们建立了热灭活金黄色葡萄球菌(HKSA)刺激的角质形成细胞的miRNA表达谱.采用荧光原位杂交(FISH)分析特应性皮炎患者中miR-939的表达。将miR-939模拟物转染至人原代角质形成细胞以研究其在体外对基质金属蛋白酶基因(MMPs)表达的影响。随后，miR-939，以及Polyplus转染试剂，给予MC903诱导的特应性皮炎皮肤以评估其体内功能。
■MiR-939在HKSA刺激的角质形成细胞和AD病变中高度上调。体外研究显示miR-939增加了基质金属蛋白酶基因的表达,包括MMP1，MMP3和MMP9，以及人原代角质形成细胞中的细胞粘附分子ICAM1。体内研究表明miR-939增加基质金属蛋白酶的表达以促进金黄色葡萄球菌的定植并加剧金黄色葡萄球菌诱导的AD样皮肤炎症。
■我们的工作揭示miR-939是AD中皮肤炎症的重要调节因子，可用作AD的潜在治疗靶点。
