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脂联素通过SIRT1介导的信号通路上调人正常角质形成细胞中的表达。

Adiponectin Upregulates Expression via SIRT1-Mediated Signaling in Human Normal Keratinocytes.

作者信息

Jin Taewon, Park Kui Young, Seo Seong Jun

机构信息

Department of Dermatology, Chung-Ang University Hospital, Seoul, Korea.

出版信息

Ann Dermatol. 2017 Aug;29(4):407-413. doi: 10.5021/ad.2017.29.4.407. Epub 2017 Jun 21.

DOI:10.5021/ad.2017.29.4.407
PMID:28761287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5500704/
Abstract

BACKGROUND

() is the major component of the epidermal granular layer and binds to and condenses the keratin cytoskeleton. thus contributes to cell compaction and serves as a natural moisturizing factor by promoting unfolding and degradation into hygroscopic amino acids. Loss or downregulation of has been shown to result in a weak stratum corneum, which causes water loss and increases the possibility of skin barrier-related seizure. Adiponectin (Acrp30) contributes to the functional recovery of somatic cells, including human normal epidermal keratinocytes (NHEKs).

OBJECTIVE

To investigate the effect of Acrp30 in expression and identifying its signal transduction mechanism.

METHODS

Normal human keratinocytes were treated with Acrp30 and the levels of were examined. Silent mating type information regulation 2 homolog (SIRT)-targeting siRNA and aryl hydrocarbon receptor nuclear translocator (ARNT)-targeting siRNA were used to identify the role of various signal transduction pathway components.

RESULTS

Acrp30 upregulated SIRT1 and ARNT expression in NHEKs, resulting in increased expression. Treatment with both SIRT1-targeting siRNA and ARNT-targeting siRNA blocked Acrp30 stimulation and silenced expression.

CONCLUSION

Adiponectin upregulates expression through a SIRT1-mediated pathway. Our results suggest that Acrp30 is a promising agent for skin barrier permeability improvement.

摘要

背景

()是表皮颗粒层的主要成分,可与角蛋白细胞骨架结合并使其浓缩。因此有助于细胞紧实,并通过促进展开和降解为吸湿氨基酸而作为一种天然保湿因子。已表明()的缺失或下调会导致角质层薄弱,从而引起水分流失并增加皮肤屏障相关癫痫发作的可能性。脂联素(Acrp30)有助于包括人正常表皮角质形成细胞(NHEK)在内的体细胞的功能恢复。

目的

研究Acrp30对()表达的影响并确定其信号转导机制。

方法

用Acrp30处理正常人角质形成细胞,并检测()的水平。使用沉默交配型信息调节2同源物(SIRT)靶向siRNA和芳烃受体核转运蛋白(ARNT)靶向siRNA来确定各种信号转导途径成分的作用。

结果

Acrp30上调了NHEK中SIRT1和ARNT的表达,导致()表达增加。用SIRT1靶向siRNA和ARNT靶向siRNA处理均阻断了Acrp30刺激并使()表达沉默。

结论

脂联素通过SIRT1介导的途径上调()表达。我们的结果表明,Acrp30是一种有前途的改善皮肤屏障通透性的药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/168aa4288349/ad-29-407-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/a1c9b4e974fe/ad-29-407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/1e7e333225b8/ad-29-407-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/fd812b9dcc01/ad-29-407-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/168aa4288349/ad-29-407-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/a1c9b4e974fe/ad-29-407-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/1e7e333225b8/ad-29-407-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/fd812b9dcc01/ad-29-407-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cb8/5500704/168aa4288349/ad-29-407-g004.jpg

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