原著 |
|
|
|
|
应用大鼠血清建立体外软骨细胞退变模型 |
王小军1, 张浩1, 詹红生2, 丁道芳2 |
1. 浙江中医药大学附属湖州市中医院骨科, 浙江 湖州 313000;
2. 上海中医药大学附属曙光医院石氏伤科医学中心, 上海 201203 |
|
Establishment of chondrocyte degeneration model in vitro by rat serum |
WANG Xiao-jun1, ZHANG Hao1, ZHAN Hong-sheng2, DING Dao-fang2 |
1. Huzhou Hospital Affiliated to Zhejiang Chinese Medical University, Huzhou 313000, China;
2. Shi's Center of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai TCM University, Shanghai 201203, China |
引用本文:
王小军, 张浩, 詹红生, 丁道芳. 应用大鼠血清建立体外软骨细胞退变模型[J]. 浙江大学学报(医学版), 2015, 44(3): 308-314.
WANG Xiao-jun, ZHANG Hao, ZHAN Hong-sheng, DING Dao-fang. Establishment of chondrocyte degeneration model in vitro by rat serum. Journal of ZheJiang University(Medical Science), 2015, 44(3): 308-314.
链接本文:
http://www.zjujournals.com/med/CN/10.3785/j.issn.1008-9292.2015.05.11
或
http://www.zjujournals.com/med/CN/Y2015/V44/I3/308
|
[1] TROEBERG L, NAGASE H. Proteases involved in cartilage matrix degradation in osteoarthritis [J]. Biochim Biophys Acta, 2012, 1824(1):133-145.
[2] LIN E A, LIU C J. The role of ADAMTSs in arthritis [J]. Protein Cell, 2010, 1(1):33-47.
[3] WU C W, TCHETINA E V, MWALE F, et al. Proteolysis involving matrix metalloproteinase 13(collagenase-3) is required for chondrocyte differentiation that is associated with matrix mineralization[J]. J Bone Miner Res, 2002, 17(4):639-651.
[4] DAHLBERG L, BILLINGHURST R C, MANNER P, et al. Selective enhancement of collagenase-mediated cleavage of resident type II collagen in cultured osteoarthritic cartilage and arrest with a synthetic inhibitor that spares collagenase 1(matrix metalloproteinase 1) [J]. Arthritis Rheum, 2000, 43(3):673-682.
[5] KOBAYASHI M, SQUIRES G R, MOUSA A, et al. Role of interleukin-1 and tumor necrosis factor alpha in matrix degradation of human osteoarthritic cartilage[J]. Arthritis Rheum, 2005, 52(1):128-135.
[6] KELLY T A, FISHER M B, OSWALD E S, et al. Low-serum media and dynamic deformational loading in tissue engineering of articular cartilage[J]. Ann Biomed Eng, 2008,36(5):769-79.
[7] MALPELI M, RANDAZZO N, CANCEDDA R, et al. Serum-free growth medium sustains commitment of human articular chondrocyte through maintenance of SOX9 expression [J]. Tissue Eng, 2004, 10(1-2):145-155.
[8] SHAO X X, DUNCAN N A, LIN L, et al. Serum-free media for articular chondrocytes in vitro expansion [J]. Chin Med J (Engl), 2013, 126(13):2523-2529.
[9] 丁道芳, 李玲慧, 宋 奕, 等. MAPK-ERK1/2信号通路调控成骨性基因表达和细胞增殖[J].南方医科大学学报, 2013, 33(10):1432-1436. DING Dao-fang, LI Ling-hui, SONG Yi, et al. MAPK-ERK1/2 signaling pathway regulates cell proliferation and osteogenic gene expression in rat osteoblasts in vitro[J]. Journal of Southern Medical University, 2013, 33(10): 1432-1436. (in Chinese)
[10] 丁道芳, 韦宋谱,李晓锋,等. 蛇床子素对大鼠原代软骨细胞增殖的抑制作用[J].中西医结合学报, 2012, 10(12):1413-1418. DING Dao-fang, WEI Song-pu, LI xiao-feng, et al. Inhibition effect of osthole on proliferation of rat chondrocytes [J]. Journal of Chinese Integrative Medicine, 2012, 10(12):1413-1418. (in Chinese)
[11] PESESSE L, SANCHEZ C, HENROTIN Y. Osteochondral plate angiogenesis: a new treatment target in osteoarthritis [J]. Joint Bone Spine, 2011, 78(2):144-149.
[12] NAGAI T, SATO M, KOBAYASHI M, et al. Bevacizumab, an anti-vascular endothelial growth factor antibody, inhibits osteoarthritis [J]. Arthritis Res Ther, 2014, 16(5):427.
[13] AIGNER T, DUDHIA J. Phenotypic modulation of chondrocytes as a potential therapeutic target in osteoarthritis: a hypothesis [J]. Ann Rheum Dis, 1997, 56(5):287-291.
[14] HO S T, YANG Z, HUI H P, et al. A serum free approach towards the conservation of chondrogenic phenotype during in vitro cell expansion [J]. Growth Factors, 2009, 27(5):321-333.
[15] PARRA-TORRES N M, C ZARES-RAGA F E, KOURI J B. Proteomic analysis of rat cartilage: the identification of differentially expressed proteins in the early stages of osteoarthritis [J]. Proteome Sci, 2014, 12(1):55.
[16] SURI S, GILL S E, MASSENA DE CAMIN S, et al. Neurovascular invasion at the osteochondral junction and in osteophytes in osteoarthritis [J]. Ann Rheum Dis, 2007, 66(11):1423-1428.
[17] AIGNER T, SACHSE A, GEBHARD P M, et al. Osteoarthritis: pathobiology-targets and ways for therapeutic intervention [J]. Adv Drug Deliv Rev, 2006, 58(2):128-149.
[18] GOLDRING M B. Update on the biology of the chondrocyte and new approaches to treating cartilage diseases [J]. Best Pract Res Clin Rheumatol, 2006, 20(5):1003-1025.
[19] USHIJIMA T, OKAZAKI K, TSUSHIMA H, et al. CCAAT/enhancer-binding protein β regulates the repression of type II collagen expression during the differentiation from proliferative to hypertrophic chondrocytes[J]. J Biol Chem, 2014, 289(5):2852-2863.
[20] SEKIYA I, TSUJI K, KOOPMAN P, et al. SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6 [J]. J Biol Chem, 2000, 275(15): 10738-10744.
[21] OKUBO Y, REDDI A H. Thyroxine downregulates SOX9 and promotes chondrocyte hypertrophy [J]. Biochem Biophys Res Commun, 2003,306(1): 186-190.
[22] RUTGERS M, SARIS D B, DHERT W J, et al. Cytokine profile of autologous conditioned serum for treatment of osteoarthritis, in vitro effects on cartilage metabolism and intra-articular levels after injection [J]. Arthritis Res Ther, 2010, 12(3):R114. |
|
Viewed |
|
|
|
Full text
|
|
|
|
|
Abstract
|
|
|
|
|
Cited |
|
|
|
|
|
Shared |
|
|
|
|
|
Discussed |
|
|
|
|