Knockdown of H19 Inhibits the Pathogenesis of Acne Vulgaris by Targeting the miR-196a/TLR2/NF-κB Axis
Knockdown of H19 Inhibits the Pathogenesis of Acne Vulgaris by Targeting the miR-196a/TLR2/NF-κB Axis
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H19 的敲低通过靶向 miR-196a/TLR2/NF-κB 轴抑制寻常痤疮的发病机制
DOI：
10.1007/s10753-020-01268-z
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发表时间：
2020-06
期刊：
影响因子：
5.1
通讯作者：
Tingting Zhu
中科院分区：
文献类型：
--
作者：
Shuyun Yang;Fumin Fang;Xiuqin Yu;Changzhi Yang;Xiaoping Zhang;Lu Wang;Liping Zhu;Kai Shao;Tingting Zhu
寻常痤疮（Acne vulgaris，AV）是一种毛囊皮脂腺单位的慢性炎症性疾病，痤疮丙酸杆菌（Propionibacterium acnes，P. acnes）与痤疮炎症有关。大量研究表明，非编码RNA在调节痤疮的病理生理过程中发挥重要作用。此外，发现的第一个印迹长非编码RNA（lncRNA）H19在炎症性疾病中起着关键作用。然而，H19在AV中的表达和作用尚不清楚。在这项研究中，我们研究了H19在角质形成细胞中的作用，并探讨了这些作用的调控机制。H19在P.痤疮呈浓度依赖性。核因子（NF）-κ B相关蛋白IκBα（p-IκBα）和p65（p-P65）的磷酸化形式在P.痤疮治疗此外，促炎细胞因子肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6和IL-8的分泌以浓度依赖性方式上调。H19的敲除抑制了P处理的角质形成细胞中p-IκBα和p-P65的表达以及TNF-α、IL-6和IL-8的分泌。粉刺。此外，发现H19通过激活NF-κB发挥其促炎作用。H19主要定位于角质形成细胞的细胞质中，通过充当miR-196 a海绵促进Toll样受体2（TLR 2）的表达。因此，H19通过miR-196 a/TLR 2轴促进NF-κB的活化和炎性细胞因子的分泌。这些发现为AV的发病机制提供了新的见解。
Acne vulgaris (AV) is a chronic inflammatory disease of the pilosebaceous unit, andPropionibacterium acnes(P. acnes) has been implicated in acne inflammation. Numerous studies have shown that non-coding RNAs play important roles in regulating the pathophysiological processes of acne. In addition, the first imprinted long non-coding RNA (lncRNA) identified, H19, plays a critical role in inflammatory disease. However, the expression and role of H19 in AV remain unclear. In this study, we investigated the effects of H19 in keratinocytes and explored the regulatory mechanisms underlying these effects. H19 was upregulated in keratinocytes treated withP. acnesin a concentration-dependent manner. The phosphorylated forms of the nuclear factor (NF)-κB-related proteins IκBα (p-IκBα) and p65 (p-P65) were significantly upregulated afterP. acnestreatment. Additionally, secretion of the proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 was upregulated in a concentration-dependent manner. Knockdown of H19 inhibited the expression of p-IκBα and p-P65 as well as the secretion of TNF-α, IL-6, and IL-8 in keratinocytes treated withP. acnes. Moreover, H19 was found to exert its proinflammatory effects by activating NF-κB. H19, which was localized mainly in the cytoplasm of keratinocytes, facilitated Toll-like receptor 2 (TLR2) expression by acting as a miR-196a sponge. H19 thus promoted the activation of NF-κB and the secretion of inflammatory cytokines through the miR-196a/TLR2 axis. These findings provide novel insight into the pathogenesis of AV.
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长非编码 RNA H19 抑制通过激活蛋白激酶 B/内皮一氧化氮抑制 miR-29b 靶基因血管内皮生长因子 a 的表达，保护内皮免受高血糖引起的炎症
DOI：
--
发表时间：
2019
期刊：
Front Cell Dev Biol
影响因子：
--
作者：
Xiao-wen Cheng;Zhen-fei Chen;Yu-feng Wan;qing zhou;yuan wang;huaqing zhu
通讯作者：
huaqing zhu
影响因子：
2.4
作者：
Hu, Yi;Li, Sukai;Zou, Yonggen
通讯作者：
Zou, Yonggen
影响因子：
5.1
作者：
Zhang, Yifeng;Yan, Jin;Zhang, Ximei
通讯作者：
Zhang, Ximei
影响因子：
1.7
作者：
T. Olszowski;I. Baranowska-Bosiacka;I. Gutowska;D. Chlubek
通讯作者：
T. Olszowski;I. Baranowska-Bosiacka;I. Gutowska;D. Chlubek
影响因子：
64.5
作者：
Kopp F;Mendell JT
通讯作者：
Mendell JT