Monocyte matrix metalloproteinase production in Type 2 diabetes and controls - a cross sectional study

被引:32
作者
Baugh, Mark D. [1 ,2 ]
Gavrilovic, Jelena [2 ]
Davies, Isabel R. [1 ,3 ]
Hughes, David A. [3 ]
Sampson, Mike J. [1 ]
机构
[1] Norfolk & Norwich Univ Hosp NHS Trust, Bertram Diabet Res Unit, Norwich NR4 7UY, Norfolk, England
[2] Univ E Anglia, Sch Biol Sci, Norwich NR4 7UA, Norfolk, England
[3] AFRC, Inst Food Res, Norwich NR4 7UA, Norfolk, England
基金
英国生物技术与生命科学研究理事会;
关键词
D O I
10.1186/1475-2840-2-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Coronary plaque rupture may result from localised over expression of matrix metalloproteinases (MMPs) within the plaque by infiltrating monocyte - macrophages. As MMP expression can be promoted by the modified lipoproteins, oxidative stress and hyperglycaemia that characterises Type 2 diabetes, we hypothesised that peripheral monocytes in these patients, exposed to these factors in vivo, would demonstrate increased MMP production compared to controls. Methods: We examined peripheral venous monocyte expression of MMP and tissue inhibitor of metalloproteinase-1 (TIMP-1) in 18 controls and 22 subjects with Type 2 diabetes and no previous cardiovascular complications. Results: No significant difference in MMP-1, 3 or 9 or TIMP-1 production was observed between control and diabetes groups. Conclusions: Monocyte MMP-1, 3, and 9, and TIMP-1, production are not abnormal in Type 2 diabetes. This data cannot be extrapolated to monocyte - macrophage behaviour in the vessel wall, but it does suggest MMP and TIMP-1 expression prior to monocyte infiltration and transformation are not abnormal in Type 2 diabetes.
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页数:4
相关论文
共 23 条
  • [1] Matrix metalloproteinase levels are elevated in inflammatory bowel disease
    Baugh, MD
    Perry, MJ
    Hollander, AP
    Davies, DR
    Cross, SS
    Lobo, AJ
    Taylor, CJ
    Evans, GS
    [J]. GASTROENTEROLOGY, 1999, 117 (04) : 814 - 822
  • [2] HMG-CoA reductase inhibitors reduce MMP-9 secretion by macrophages
    Bellosta, S
    Via, D
    Canavesi, M
    Pfister, P
    Fumagalli, R
    Paoletti, R
    Bernini, F
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (11) : 1671 - 1678
  • [3] Borch-Johnsen K, 1999, LANCET, V354, P617
  • [4] Braschi S, 2001, DIABETOLOGIA, V44, pA321
  • [5] MONOCLONAL-ANTIBODIES AGAINST HUMAN FIBROBLAST COLLAGENASE AND THE DESIGN OF AN ENZYME-LINKED-IMMUNOSORBENT-ASSAY TO MEASURE TOTAL COLLAGENASE
    CLARK, IM
    POWELL, LK
    WRIGHT, JK
    CAWSTON, TE
    HAZLEMAN, BL
    [J]. MATRIX, 1992, 12 (06): : 475 - 480
  • [6] Normalization of plasma lipid peroxides, monocyte adhesion, and tumor necrosis factor-α production in NIDDM patients after gliclazide treatment
    Desfaits, AC
    Serri, O
    Renier, G
    [J]. DIABETES CARE, 1998, 21 (04) : 487 - 493
  • [7] Increased plasma metalloproteinase-9 concentrations precede development of microalbuminuria in non-insulin-dependent diabetes mellitus
    Ebihara, I
    Nakamura, T
    Shimada, N
    Koide, H
    [J]. AMERICAN JOURNAL OF KIDNEY DISEASES, 1998, 32 (04) : 544 - 550
  • [8] ENDEMANN G, 1993, J BIOL CHEM, V268, P11811
  • [9] INCREASED EXPRESSION OF MATRIX METALLOPROTEINASES AND MATRIX-DEGRADING ACTIVITY IN VULNERABLE REGIONS OF HUMAN ATHEROSCLEROTIC PLAQUES
    GALIS, ZS
    SUKHOVA, GK
    LARK, MW
    LIBBY, P
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1994, 94 (06) : 2493 - 2503
  • [10] Matrilysin is expressed by lipid-laden macrophages at sites of potential rupture in atherosclerotic lesions and localizes to areas of versican deposition, a proteoglycan substrate for the enzyme
    Halpert, I
    Sires, UI
    Roby, JD
    PotterPerigo, S
    Wight, TN
    Shapiro, SD
    Welgus, HG
    Wickline, SA
    Parks, WC
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (18) : 9748 - 9753