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新型小管间质性纤维化中周细胞-肌成纤维细胞转化的机制：核心岩藻糖基化调控。

Novel Mechanism of the Pericyte-Myofibroblast Transition in Renal Interstitial Fibrosis: Core Fucosylation Regulation.

机构信息

Department of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.

Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Fuxing Road 28, Haidian District, Beijing, 100853, China.

出版信息

Sci Rep. 2017 Dec 5;7(1):16914. doi: 10.1038/s41598-017-17193-5.

DOI:10.1038/s41598-017-17193-5
PMID:29209018
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5717002/
Abstract

Pericytes have been identified as a major source of myofibroblasts in renal interstitial fibrosis (RIF). The overactivation of several signaling pathways, mainly the TGF-β and PDGF pathways, initiates the pericyte-myofibroblast transition during RIF. Key receptors in these two pathways have been shown to be modified by fucosyltransferase 8 (FUT8), the enzyme that catalyzes core fucosylation. This study postulated that core fucosylation might play an important role in regulating the pericyte transition in RIF. The data showed that core fucosylation increased with the extent of RIF in patients with IgA nephropathy (IgAN). Similarly, core fucosylation of pericytes increased in both a unilateral ureteral occlusion (UUO) mouse model and an in vitro model of pericyte transition. Inhibition of core fucosylation by adenoviral-mediated FUT8 shRNA in vivo and FUT8 siRNA in vitro significantly reduced pericyte transition and RIF. In addition, the activation of both the TGF-β/Smad and PDGF/ERK pathways was blocked by core fucosylation inhibition. In conclusion, core fucosylation may regulate the pericyte transition in RIF by modifying both the TGF-β/Smad and PDGF/ERK pathways. Glycosylation might be a novel "hub" target to prevent RIF.

摘要

周细胞已被确定为肾间质纤维化（RIF）中肌成纤维细胞的主要来源。在 RIF 期间，几种信号通路（主要是 TGF-β 和 PDGF 通路）的过度激活引发周细胞-肌成纤维细胞转化。这两条通路中的关键受体已被证明被岩藻糖基转移酶 8（FUT8）修饰，该酶催化核心岩藻糖基化。本研究假设核心岩藻糖基化可能在调节 RIF 中的周细胞转化中发挥重要作用。数据显示，在 IgA 肾病（IgAN）患者中，核心岩藻糖基化随着 RIF 的严重程度而增加。同样，在单侧输尿管梗阻（UUO）小鼠模型和周细胞转化的体外模型中，周细胞的核心岩藻糖基化均增加。体内通过腺病毒介导的 FUT8 shRNA 和体外 FUT8 siRNA 抑制核心岩藻糖基化显著减少了周细胞转化和 RIF。此外，核心岩藻糖基化抑制阻断了 TGF-β/Smad 和 PDGF/ERK 通路的激活。总之，核心岩藻糖基化可能通过修饰 TGF-β/Smad 和 PDGF/ERK 通路来调节 RIF 中的周细胞转化。糖基化可能是预防 RIF 的新型“枢纽”靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/7bbedb692cdb/41598_2017_17193_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/351c20279d4f/41598_2017_17193_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/7ddf06533e67/41598_2017_17193_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/7bbedb692cdb/41598_2017_17193_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/351c20279d4f/41598_2017_17193_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/33ddb59ffe4f/41598_2017_17193_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/d7add7a4b06b/41598_2017_17193_Fig3_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/bd3ce6137818/41598_2017_17193_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/7ddf06533e67/41598_2017_17193_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6a7/5717002/7bbedb692cdb/41598_2017_17193_Fig7_HTML.jpg

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