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抵抗素通过角蛋白8激活p65信号通路并降低糖原含量。

Resistin Activates p65 Pathway and Reduces Glycogen Content through Keratin 8.

作者信息

Wen Fengyun, Xia Qiao, Zhang Hui, Shia Haipeng, Rajesh Amin, Wu Yanling, Yang Yi, Yang Zaiqing

机构信息

College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, Henan, China.

Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430070, Hubei, China.

出版信息

Int J Endocrinol. 2020 May 18;2020:9767926. doi: 10.1155/2020/9767926. eCollection 2020.

DOI:10.1155/2020/9767926
PMID:32508919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7251471/
Abstract

Resistin is associated with metabolic syndrome and inflammatory conditions. Many studies have suggested that resistin inhibits the accumulation of glycogen; however, the exact mechanisms of resistin-induced decrease in glycogen content remain unclear. Keratin 8 is a typical epithelial intermediate filament protein, but numerous studies suggest a vital role of K8 in glucose metabolism. However, it is still not known whether K8 participates in the mediation of resistin-induced reduction of cellular glycogen accumulation. In this study, we found that resistin upregulated expression of the p65 subunit of NF-B, which led to the promotion of K8 transcriptional expression; in turn, the expression of K8 inhibited glycogen accumulation in HepG2 cells.

摘要

抵抗素与代谢综合征及炎症状态相关。许多研究表明,抵抗素会抑制糖原积累;然而,抵抗素导致糖原含量降低的确切机制仍不清楚。角蛋白8是一种典型的上皮中间丝蛋白,但众多研究表明K8在葡萄糖代谢中起重要作用。然而,K8是否参与介导抵抗素诱导的细胞糖原积累减少尚不清楚。在本研究中,我们发现抵抗素上调了NF-κB p65亚基的表达,这导致K8转录表达的促进;反过来,K8的表达抑制了HepG2细胞中的糖原积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/332c812869bf/IJE2020-9767926.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/19589f1d9772/IJE2020-9767926.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/b5a2ec75b890/IJE2020-9767926.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/9ce91002a63e/IJE2020-9767926.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/b5b3937b77e9/IJE2020-9767926.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/332c812869bf/IJE2020-9767926.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/19589f1d9772/IJE2020-9767926.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/b5a2ec75b890/IJE2020-9767926.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/9ce91002a63e/IJE2020-9767926.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/b5b3937b77e9/IJE2020-9767926.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f66/7251471/332c812869bf/IJE2020-9767926.005.jpg

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本文引用的文献

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Biosci Biotechnol Biochem. 2016 Jul;80(7):1313-20. doi: 10.1080/09168451.2016.1153951. Epub 2016 Feb 29.
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Prevalence of genetic variants of keratins 8 and 18 in patients with drug-induced liver injury.药物性肝损伤患者中角蛋白8和18基因变异的患病率。
BMC Med. 2015 Aug 19;13:196. doi: 10.1186/s12916-015-0418-0.
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Keratin 8 absence down-regulates colonocyte HMGCS2 and modulates colonic ketogenesis and energy metabolism.
角蛋白8缺失会下调结肠细胞中的HMGCS2,并调节结肠生酮作用和能量代谢。
Mol Biol Cell. 2015 Jun 15;26(12):2298-310. doi: 10.1091/mbc.E14-02-0736. Epub 2015 Apr 22.
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In stage II/III lymph node-positive breast cancer patients less than 55 years of age, keratin 8 expression in lymph node metastases but not in the primary tumour is an indicator of better survival.在年龄小于55岁的II/III期淋巴结阳性乳腺癌患者中,淋巴结转移灶而非原发肿瘤中的角蛋白8表达是生存情况较好的一个指标。
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Keratins and skin disease.角蛋白与皮肤病。
Cell Tissue Res. 2015 Jun;360(3):583-9. doi: 10.1007/s00441-014-2105-4. Epub 2015 Jan 27.
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Association between metabolic syndrome, obesity, diabetes mellitus and oncological outcomes of bladder cancer: a systematic review.代谢综合征、肥胖、糖尿病与膀胱癌肿瘤学结局之间的关联:一项系统评价
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MiRNA-145 is involved in the development of resistin-induced insulin resistance in HepG2 cells.miRNA-145 参与抵抗素诱导的 HepG2 细胞胰岛素抵抗的发生。
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