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抗抑瘤素M抗体抑制狼疮性肾炎小鼠模型中的肾小管间质病变。

Anti-OSM Antibody Inhibits Tubulointerstitial Lesion in a Murine Model of Lupus Nephritis.

作者信息

Liu Qingjuan, Du Yunxia, Li Kejun, Zhang Wei, Feng Xiaojuan, Hao Jun, Li Hongbo, Liu Shuxia

机构信息

Department of Pathology, Key Laboratory of Kidney Diseases of Hebei Province, Hebei Medical University, Shijiazhuang, Hebei 050017, China.

Department of Ophthalmology, People's Hospital of Hebei Province, Shijiazhuang, Hebei 050000, China.

出版信息

Mediators Inflamm. 2017;2017:3038514. doi: 10.1155/2017/3038514. Epub 2017 May 24.

DOI:10.1155/2017/3038514
PMID:28626343
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5463100/
Abstract

The purpose of this study was to investigate the role of oncostatin M (OSM) in tubulointerstitial lesion (TIL) in lupus nephritis (LN). We found that OSM was highly expressed in the renal tissue of LN mice. OSM is one of the interleukin-6 cytokine family members. In order to clarify the role and mechanism of OSM in LN, mice with LN were treated with anti-OSM antibody or isotype antibody. We evaluated the tubular epithelial-mesenchymal transdifferentiation (EMT) by detecting the E-cadherin, -smooth muscle actin (-SMA), and fibronectin (FN) expression. We analyzed the inflammation by observing the monocyte chemotactic factor-1 (MCP-1) and intercellular adhesion molecule (ICAM-1) expression and calculated the tubulointerstitial fibrosis area by Masson staining. The results showed that anti-OSM antibody, rather than isotype antibody, improved EMT, inflammation, and tubulointerstitial fibrosis. In addition, the signal transducer and activator of transcription (STAT) 1 and STAT3 signaling was activated by tyrosine phosphorylation in LN mouse renal tissue, indicating that the phosphorylated STAT1 (p-STAT1) and p-STAT3 were involved in kidney injury. Moreover, decreased p-STAT3 instead of p-STAT1 has been observed after anti-OSM antibody injection. Thus, we concluded that OSM is associated with TIL in lupus nephritis, which may be connected with the activation of STAT3 rather than that of STAT1.

摘要

本研究旨在探讨抑瘤素M（OSM）在狼疮性肾炎（LN）肾小管间质病变（TIL）中的作用。我们发现OSM在LN小鼠的肾组织中高表达。OSM是白细胞介素-6细胞因子家族成员之一。为了阐明OSM在LN中的作用及机制，用抗OSM抗体或同型抗体处理LN小鼠。我们通过检测E-钙黏蛋白、α-平滑肌肌动蛋白（α-SMA）和纤连蛋白（FN）的表达来评估肾小管上皮-间充质转分化（EMT）。通过观察单核细胞趋化因子-1（MCP-1）和细胞间黏附分子（ICAM-1）的表达来分析炎症，并通过Masson染色计算肾小管间质纤维化面积。结果显示，抗OSM抗体而非同型抗体改善了EMT、炎症和肾小管间质纤维化。此外，LN小鼠肾组织中信号转导子和转录激活子（STAT）1和STAT3信号通过酪氨酸磷酸化被激活，表明磷酸化的STAT1（p-STAT1）和p-STAT3参与了肾损伤。而且，注射抗OSM抗体后观察到p-STAT3而非p-STAT1减少。因此，我们得出结论，OSM与狼疮性肾炎中的TIL相关，这可能与STAT3而非STAT1的激活有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/05a870ee8406/MI2017-3038514.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/d922c87c70f5/MI2017-3038514.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/0c92103148ed/MI2017-3038514.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/6ca4d8e51e2e/MI2017-3038514.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/ec6c00987cbd/MI2017-3038514.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/a6d87abf79b5/MI2017-3038514.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/05a870ee8406/MI2017-3038514.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/d922c87c70f5/MI2017-3038514.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/0c92103148ed/MI2017-3038514.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/6ca4d8e51e2e/MI2017-3038514.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/ec6c00987cbd/MI2017-3038514.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/a6d87abf79b5/MI2017-3038514.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f1a/5463100/05a870ee8406/MI2017-3038514.006.jpg

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