[1]曾文波,兰生辉,蔡贤华,等.EGFR信号通路在骨性关节炎研究中进展[J].中华老年骨科与康复电子杂志,2019,(02):109-113.[doi:10.3877/cma.j.issn.2096-0263.2019.02.009]
 Zeng Wenbo,Lan Shenghui,Cai Xianhua,et al.Progress of the role of EGFR signaling pathway in osteoarthritis[J].Chin J Geriatr Orthop Rehabil(Electronic Edition),2019,(02):109-113.[doi:10.3877/cma.j.issn.2096-0263.2019.02.009]
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EGFR信号通路在骨性关节炎研究中进展()
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中华老年骨科与康复电子杂志[ISSN:1674-3911/CN:11-9292/R]

卷:
期数:
2019年02期
页码:
109-113
栏目:
综述
出版日期:
2019-04-05

文章信息/Info

Title:
Progress of the role of EGFR signaling pathway in osteoarthritis
作者:
曾文波12兰生辉12蔡贤华12刘曦明12
430070 武汉,中国人民解放军中部战区总医院骨科(湖北省骨创伤救治临床医学研究中心)1;510515 广州,南方医科大学2
Author(s):
Zeng Wenbo12 Lan Shenghui12 Cai Xianhua12 Liu Ximing12
1Depatment of Othopedics, Central theater command General Hospital of the PLA (Clinical Medical Research Center for Bone Trauma Treatment in Hubei Province), Wuhan 430070, China;2Southern Medical University, Guangzhou 510515, China
关键词:
受体表皮生长因子 骨性关节炎 软骨细胞 生物学作用
Keywords:
Receptor epidermal growth factor Osteoarthritis Chondrocytes Biological functions
DOI:
10.3877/cma.j.issn.2096-0263.2019.02.009
文献标志码:
A
摘要:
软骨细胞在骨关节表面形成保护关节的软骨组织,关节软骨细胞的增殖、分化、凋亡及代谢的失衡将导致骨性关节炎(OA)的发生。近年研究发现,表皮生长因子受体(EGFR)信号通路是多功能细胞因子,与人体多种器官和组织的病理及生理过程紧密相关,在调节软骨细胞的生长及代谢过程中发挥重要作用。因此,本文围绕OA病变中EGFR信号通路在OA中的作用和机制进行综述,以期为OA和其他骨关节疾病的研究和治疗提供新的方法和思路。
Abstract:
Chondrocytes form articular cartilage on the surface of arthrosis. The proliferation, differentiation, apoptosis and metabolic imbalance of articular chondrocytes will lead to the occurrence of osteoarthritis (OA). Recent studies have shown that EGFR signaling pathway is a multifunctional cytokine, which is closely related to the pathological and physiological processes of various organs and tissues, and plays an important role in regulating the growth and metabolism of chondrocytes. Therefore, this review focuses on the role and mechanism of EGFR signaling pathway in OA, in order to provide new methods and ideas for the research and treatment of OA and other bone and joint diseases.

参考文献/References:

1 Vos T, Flaxman AD, Naghavi M, et al. Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010 [J]. Lancet, 2012, 380(9859): 2163-2196.
2 Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the Global Burden of Disease 2010 study [J]. Ann Rheum Dis, 2014, 73(7): 1323-1330.
3 Long DL, Ulici V, Chubinskaya S, et al. Heparin-binding epidermal growth factor-1ike growth factor(HB-EGF)is increased in osteoarthritis and regulates chondrocyte catabolic and anabolic activities [J]. Osteoarthritis Cartilage, 2015, 23(9): 1523-1531.
4 Jia H, Ma X, Tong W, et al. EGFR signaling is critical for maintaining the superficial layer of articularcartilage and preventing osteoarthritis initiation [J]. Proc Natl Acad Sci U S A, 2016, 113(50): 14360-14365.
5 Mobasheri A, Bondy CA, Moley, et al. Facilitative glucose transporters in articular chondrocytes. Expression, distribution and functional regulation of GLUT isoforms by hypoxia, hypoxia mimetics, growth factors and pro-inflammatory cytokines[J]. Adv Anat Embryol Cell Biol,2008,200:1p following vi, 1-84.
6 Buckwalter JA, Mankin HJ, Grodzinsky AJ. Articular cartilage and osteoarthritis[J].Instr Course Lect, 2005, 54:465-480.
7 Felson DT, Neogi T.Osteoarthritis: is it a disease of cartilage or of bone?[J]. Arthritis Rheum, 2004, 50(2):341-344.
8 Schneider MR, Sibilia M, Erben RG. The EGFR network in bone biology and pathology [J]. Trends EndocrinolMetab, 2009, 20(10): 517-524.
9 Schneider MR, Wolf E. The epidermal growth factor receptor ligands at a glance [J]. J Cell Physiol, 2009, 218(3): 460-466.
10 AppletonCT, UsmaniSE, MortJS, et al. Rho/ROCK and MEK/ERK activation by transforminggrowth factor-a induces articular cartilage degradation[J]. Lab Invest, 2010,90(1): 20-30.
11 袁功武, 兰生辉, 刘曦明. 表皮生长因子受体信号通路对骨折愈合的生物学作用 [J]. 中国矫形外科杂志, 2018, 26(4): 328-332.
12 袁功武, 兰生辉, 曾文波, 等. 吉非替尼对骨折愈合中I,II 及X 型胶原基因表达的影响 [J]. 中国矫形外科杂志, 2018, 26(10): 939-944.
13 Gschwind A, Fischer OM, Ullrich A. The discovery of receptor tyrosine kinases: targets for cancer therapy [J]. Nat Rev Cancer, 2004, 4(5): 361-370.
14 Zhang X, Zhu J, Liu F, et al. Reduced EGFR signaling enhances cartilage destruction in a mouse osteoarthritis model [J]. Bone Res, 2014,5(2): 14015.
15 Pest MA, Russell BA, Zhang YW, et al. Disturbed cartilage and joint homeostasis resulting from a loss of Mitogen-Inducible gene 6 in a mouse model of joint dysfunction [J]. Arthritis Rheumatol, 2014, 66(10): 2816-2827.
16 Shepard JB, Jeong JW, Maihle NJ, et al. Transient anabolic effects accompany epidermal growth factor receptor signal activation in articular cartilage in vivo [J]. Arthritis Res Ther, 2013, 15(3): R60.
17 Staal B, Williams BO, Beier F, et al. Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation [J]. Proc Natl Acad Sci U S A, 2014, 111(7): 2590-2595.
18 Roskoski R Jr. ERK1/2 MAP kinases: structure, function, and regulation [J]. Pharmacol Res, 2012, 66(2): 105-143.
19 He P, Shen N, Gao G, et al. Periodic mechanical stress activates PKC delta-Dependent EGFR mitogenic signals in rat chondrocytes via PI3K-Akt and ERK1/2 [J]. Cell Physiol Biochem, 2016, 39(4): 1281-1294.
20 Naik B, Kumar M, Khanna AK, et al. Clinico-histopathological study of varicose vein and role of matrix metalloproteinases-1,matrix metalloproteinases-9 and tissue inhibitor of matrix metalloproteinase-1 in varicose vein formation [J]. Indian J Pathol Microbiol, 2016, 59(1): 25-30.
21 Konstantinos C Tsolis, Ekaterini S Bei, Ioanna Papathanasiou,et al. Comparative proteomic analysis of hypertrophicchondrocytes in osteoarthritis[J].Clin Proteomics,2015,12(1):12.
22 Gehris AL, Stringa E, Spina J, et al. The region encoded by the alternatively splicedexon IIIA in mesenchymal fibronectin appears essential forchondrogenesis at the level of cellular condensation[J]. Dev Biol, 1997,190(2): 191-205.
23 Takeda H, Inoue H, Kutsuna T,et al. Activation of epidermal growth factor receptor gene is involvedin transforming growth factor-?mediated fibronectinexpression in a chondrocyte progenitor cell line[J]. Int J Mol Med,2010,25(4): 593-600.
24 刘艳, 尹若峰, 侯睿智. BMP-2诱导软骨细胞凋亡及增殖的研究 [J]. 中华骨与关节外科杂志, 2016, 9(03): 251-254.
25 Goggs R, Carter SD, Schulze-Tanzil G, et al. Apoptosis and the loss of chondrocyte survival signals contribute to articular cartilage degradation in osteoarthritis [J]. Vet J, 2003, 166(2): 140-158.
26 So T, Croft M. Regulation of PI-3-kinase and Akt signaling in T lymphocytes and other cells by TNFR family molecules [J]. Front Immunol, 2013, 4: 139.
27 ShengZG, HuangW, LiuYX, et al.Ofloxacin induces apoptosis via β1 integrin-EGFR-Rac1-Nox2 pathway inmicroencapsulated chondrocytes[J]. Toxicol Appl Pharmacol, 2013,267(1):74-87.
28 Goldring MB, Goldring SR. Articular cartilage and subchondral bone in the pathogenesis of osteoarthritis[J].Ann N Y Acad Sci, 2010. 1192: 230-237.
29 Piel MJ, Kroin JS, Im HJ. Assessment of knee joint pain in experimental rodentmodels of osteoarthritis[J]. Methods Mol Biol, 2015,1226:175-181.
30 Henry SP, Jang CW, Deng JM, et al. Generation of aggrecan-CreERT2 knockin mice for inducibleCre activity in adult cartilage [J]. Genesis, 2009, 47(12): 805-814.
31 Zhang X, Zhu J, Liu F, et al. Reduced EGFR signaling enhances cartilage destruction in a mouse osteoarthritis model [J]. Bone Res, 2014,5(2): 14015.][Henry SP, Jang CW, Deng JM, et al. Generation of aggrecan-CreERT2 knockin mice for inducibleCre activity in adult cartilage [J]. Genesis, 2009, 47(12): 805-814.
32 Bonnevie ED, Galesso D, Secchieri C, et al. Elastoviscous transitions of articular cartilage reveal a mechanism of synergy between lubricin and hyaluronic acid [J]. PLoS One, 2015, 10(11): e0143415.
33 Das S, Banquy X, Zappone B, et al. Synergistic interactions between grafted hyaluronic acid and lubricin provide enhanced wear protection and lubrication [J]. Biomacromolecules, 2013, 14(5): 1669-1677.
34 Lim H, Kim HP. Matrix metalloproteinase-13 expression in IL-1β-treated chondrocytes by activation of the p38 MAPK/c-Fos/AP-1 and JAK/STAT pathways [J]. Arch Pharm Res, 2011, 34(1): 109-117.
35 Long DL, Loeser RF. p38gamma mitogen-activated protein kinase suppresses chondrocyte production of MMP-13 in response to catabolic stimulation [J]. Osteoarthritis Cartilage, 2010, 18(9): 1203-1210.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金资助项目(81601902);湖北省自然科学基金(2015CFB240);博士后科学基金(2015M572817);湖北省自然科学基金专项(2017ACA099);湖北省卫生和计划生育委员会联合基金项目(WJ2018H0064)
更新日期/Last Update: 2019-04-12