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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:

25卷

期数:

2019年02期

页码:

115-118

栏目:

基础医学

出版日期:

2019-03-20

文章信息/Info

Title:

Effects of miR-145-5p on joint inflammation in collagen-induced arthritis mice

文章编号:

1006-8147(2019)02-0115-04

作者:

明建松¹; 2; 王晓雪¹; 杨梦晨¹; 汤 可¹; 袁玉华¹

（1.天津医科大学总医院检验科，天津 300052；2.天津港口医院检验科，天津 300456）

Author(s):

MING Jian-song¹; 2;  WANG Xiao-xue¹;  YANG Meng-chen¹;  TANG Ke¹;  YUAN Yu-hua¹

（1.Department of Chinical Laboratory, General Hospital, Tianjin Medical University, Tianjin 300052, china；2. Department of Clinical Laboratory, Tianjin Port Hospital, Tianjin 300456，China）

关键词:

类风湿关节炎; microRNA ; 胶原诱导关节炎模型

Keywords:

rheumatoid arthritis;  microRNA;  collagen-induced arthritis model

分类号:

R684.3

DOI:

-

文献标志码:

A

摘要:

目的：探讨miR-145-5p对胶原诱导的关节炎（CIA）小鼠关节变化的影响。方法：采用牛Ⅱ型胶原免疫DBA/1小鼠诱导CIA，对关节指数评分及足跖肿胀程度进行比较，成模后随机分为agomiR-145-5p组和agomiR空载体（agomiR-NC）组进行干扰，采用足爪micro-CT摄片，踝关节病理检查评分及石蜡切片、HE染色进行处理，并通过免疫组化方法（IHC）检测踝关节中金属蛋白酶-1（MMP-1）、金属蛋白酶-3（MMP-3）、金属蛋白酶-9（MMP-9）、金属蛋白酶-13（MMP-13）、白细胞介素17（IL-17）和金属蛋白酶17（ADAM17）的表达。结果：成功建立CIA小鼠模型，与agomiR-NC组相比，agomiR-145-5p组micro-CT分析显示骨侵蚀更严重，组织病理学显示滑膜炎症减轻，免疫组化结果显示MMP-3、MMP-9、MMP-13和IL-17水平升高， MMP-1水平无差异，ADAM17水平降低（P<0.05）。结论：成功建立CIA小鼠模型，并发现miR-145-5p加重关节破坏的同时部分抑制了CIA小鼠的关节炎症。

Abstract:

Objective: To investigate the effect of miR-145-5p on joint changes in collagen-induced arthritis (CIA) mice. Methods：The CIA was induced by immunization of bovine type II collagen in DBA/1 mice, and the joint index scores and degree of paw swelling were compared. After the model was formed, they were randomly divided into agomiR-145-5p group and agomiR-NC group toperform interference.Foot micro-CT radiographs, ankle pathology score, paraffin sections, and HE staining were measured. IHC was used to detect the expression of MMP-1, MMP-3, MMP-9, MMP-13, IL-17 and ADAM17 in the ankle joint. Results：The CIA mouse model was successfully established. Compared with the agomiR-NC group, bone erosion was more severe in the agomiR-145-5p group. Histopathology showed synovial inflammation was reduced, and immunohistochemistry showed MMP-3 and MMP-9, MMP-13 and IL-17 levels increased, MMP-1 levels were not different, and ADAM17 levels decreased (P<0.05). Conclusion： We have successfully established a CIA mouse model and found that miR-145-5p could aggravate joint destruction while partially inhibiting joint inflammation in CIA mice.

参考文献/References:

[1] 闫琛. miR-145-5p在类风湿关节炎中的表达及功能研究[D].天津医科大学，2017
[2] Bakharevski O, Stein-Oakley A N, Thomson N M, et al.Collagen induced arthritis in rats.Contrasting effect of subcutaneous versus intradermal inoculation of type II collagen[J]. J Rheumatol,1998, 25（10）:1945
[3] Shen H, Li L, Zhou S, et al.The role of ADAM17 in tumorigenesis and progression of breast cancer[J]. Tumour Biol, 2016,37:15359
[4] Siney E J, Holden A, Casselden E, et al. Metalloproteinases ADAM10 and ADAM17 Mediate Migration and Differentiation in Glioblastoma Sphere-Forming Cells[J].Mol Neurobiol, 2016,54（5）:3893
[5] Nagatani K, Itoh K, NakajimaK,et al.Rheumatoid arthritis fibroblast-like synoviocytes express BCMA and are stimulated by APRIL[J]. Arthritis Rheum,2007,56（11）:3554
[6] Lefebvre J S, Lévesque T, Picard S, et al. Extra domain A of fibronectin primes leukotriene biosynthesis and stimulates neutrophil migration through activation of Toll-like receptor 4[J]. Arthritis Rheum, 2011,63（6）:1527
[7] Mori J, Patel VB, AboAlrob O, et al. Angiotensin 1-7 ameliorates diabetic cardiomyopathy and diastolic dysfunction in db/db mice by reducing lipotoxicity and inflammation[J]. Circ Heart Fail,2014, 7（2）: 327
[8] Pizzo R J, Azadniv M, Guo N, et al. Phenotypic,genotypic,and functional characterization of normal and acute myeloid leukemia-derived marrow endothelial cells[J]. Exp Hematol,2016,44（5）:378
[9] Zhu S, Qian Y. IL-17/IL-17 receptor system in autoimmune disease: mechanisms and therapeutic potential[J]. Clin Sci,2012,122（11）:487
[10] Veldhoen M. Interleukin 17 is a chief orchestrator of immunity[J]. Nat Immunol, 2017,18（6）:612
[11] Varas A, Valencia J, Lavocat F, et al. Blockade of bone morphogenetic protein signaling potentiates the pro-inflammatory phenotype induced by interleukin-17 and tumor necrosis factor-α combination in rheumatoid synoviocytes[J]. Arthritis Res Ther, 2015,17:192
[12] Li G, Zhang Y, Qian Y, et al. Interleukin-17A promotes rheumatoid arthritis synoviocytes migration and invasion under hypoxia by increasing MMP2 and MMP9 expression through NF-κB/HIF-1α pathway[J]. Mol Immunol, 2013,53（3）:227
[13] Lubberts E, Joosten L A, van de Loo F A, et al. Overexpression of IL-17 in the knee joint of collagen type II immunized mice promotes collagen arthritis and aggravates joint destruction[J]. InflammRes, 2002,51（2）:102
[14] Seddiki N, Brezar V, Ruffin N, et al. Role of miR-155 in the regulation of lymphocyte immune function and disease[J].Immunology, 2014, 142（1）: 32
[15] Zhang X, Li D, Li M, et al. MicroRNA-146a targets PRKCE to modulate papillary thyroid tumor development[J]. Int J Cancer,2014,134（2）: 257

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备注/Memo

备注/Memo:

作者简介 明建松（1987-），男，硕士在读，研究方向：病原生物学；通信作者：袁玉华，E-mail：yyhxxx39@sina.com。

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更新日期/Last Update: 2019-04-25