Expression of Genes Encoding Matrix Metalloproteinases (MMPs) and their Tissue Inhibitors (TIMPs) in Normal and Diseased Canine Mitral Valves

被引:31
作者
Aupperle, H. [1 ]
Thielebein, J. [2 ]
Kiefer, B. [2 ]
Maerz, I. [3 ]
Dinges, G.
Schoon, H. -A. [1 ]
Schubert, A. [4 ]
机构
[1] Univ Leipzig, Fac Vet Med, Inst Vet Pathol, D-04103 Leipzig, Germany
[2] Univ Halle Wittenberg, Inst Agr & Ernahrungswissensch, D-06108 Halle, Germany
[3] Univ Leipzig, Fac Vet Med, Klin Kleintiere, D-04103 Leipzig, Germany
[4] Fraunhofer Inst Zelltherapie & Immunol, D-04103 Leipzig, Germany
关键词
dog; heart valve; matrix metalloproteinase; tissue inhibitor of matrix metalloproteinase; MYXOMATOUS DEGENERATION; VALVULAR DISEASE; HEART-VALVES; DOGS; LEAFLETS; MT1-MMP; BINDING;
D O I
10.1016/j.jcpa.2009.01.001
中图分类号
R36 [病理学];
学科分类号
100103 [病原生物学];
摘要
The pathogenesis of canine chronic valvular disease (CVD) is not fully characterized. The present study investigates the expression of genes encoding matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in normal and diseased mitral valves (MVs). Samples from normal (n = 15) or diseased (n = 10) canine MVs were subject to real-time polymerase chain reaction (PCR) for quantification of mRNA encoding MMP-1, -2, -9 and -14 and TIMP-2, -3 and -4. In normal valves there was low expression of mRNA encoding MMP-2, -9 and -14 and TIMP-3. In the valves from dogs with CVD there was significantly increased transcription of mRNA encoding MMP-1 and -14 and TIMP-2, -3 and -4, but no elevation in mRNA encoding MMP-2 and -9. MMps and TIMPs are therefore likely to be involved in extracellular matrix metabolism in canine MVs and there are significant alterations in the expression of genes encoding these molecules during CVD. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:271 / 277
页数:7
相关论文
共 23 条
[1]
An immunohistochemical study of the role of matrix metalloproteinases and their tissue inhibitors in chronic mitral valvular disease (valvular endocardiosis) in dogs [J].
Aupperle, Heike ;
Thielebein, Jens ;
Kiefer, Birgit ;
Maerz, Imke ;
Dinges, Gregor ;
Schoon, H. -A. .
VETERINARY JOURNAL, 2009, 180 (01) :88-94
[2]
Specific, high affinity binding of tissue inhibitor of metalloproteinases-4 (TIMP4) to the COOH-terminal hemopexin-like domain of human gelatinase A - TIMP-4 binds progelatinase A and the COOH-terminal domain in a similar manner to TIMP-2 [J].
Bigg, HF ;
Shi, YE ;
Liu, YLE ;
Steffensen, B ;
Overall, CM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (24) :15496-15500
[3]
Ultrastructural morphologic evaluation of the phenotype of valvular interstitial cells in dogs with myxomatous degeneration of the mitral valve [J].
Black, A ;
French, AT ;
Dukes-McEwan, J ;
Corcoran, BM .
AMERICAN JOURNAL OF VETERINARY RESEARCH, 2005, 66 (08) :1408-1414
[4]
Borgarelli Michele, 2004, J Vet Cardiol, V6, P27, DOI 10.1016/S1760-2734(06)70055-8
[5]
Buchanan J W, 1977, Adv Vet Sci Comp Med, V21, P75
[6]
Identification of surface morphologic changes in the mitral valve leaflets and chordae tendineae of dogs with myxomatous degeneration [J].
Corcoran, BM ;
Black, A ;
Anderson, H ;
McEwan, JD ;
French, A ;
Smith, P ;
Devine, C .
AMERICAN JOURNAL OF VETERINARY RESEARCH, 2004, 65 (02) :198-206
[7]
Dreger SA, 2002, J HEART VALVE DIS, V11, P875
[8]
Extracellular matrix remodelling in human aortic valve disease: the role of matrix metalloproteinases and their tissue inhibitors [J].
Fondard, O ;
Detaint, D ;
Lung, B ;
Choqueux, C ;
Adle-Biassette, H ;
Jarraya, M ;
Hvass, U ;
Couetil, JP ;
Henin, D ;
Michel, JB ;
Vahanian, A ;
Jacob, MP .
EUROPEAN HEART JOURNAL, 2005, 26 (13) :1333-1341
[9]
Grüninger E, 1998, J COMP PATHOL, V119, P293, DOI 10.1016/S0021-9975(98)80051-0
[10]
New insights into degenerative mitral valve disease in dogs [J].
Häggström, J ;
Pedersen, HD ;
Kvart, C .
VETERINARY CLINICS OF NORTH AMERICA-SMALL ANIMAL PRACTICE, 2004, 34 (05) :1209-+