|本期目录/Table of Contents|

[1]明建松,王晓雪,杨梦晨,等.MiR-145-5p对胶原诱导的关节炎小鼠关节炎症的影响[J].天津医科大学学报,2019,25(02):115-118.
 MING Jian-song,WANG Xiao-xue,YANG Meng-chen,et al.Effects of miR-145-5p on joint inflammation in collagen-induced arthritis mice[J].Journal of Tianjin Medical University,2019,25(02):115-118.
点击复制

MiR-145-5p对胶原诱导的关节炎小鼠关节炎症的影响(PDF)
分享到:

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

卷:
25
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12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-song12 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

相似文献/References:

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。
更新日期/Last Update: 2019-04-25