Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice
Departments of 1 Pathology and 3 Pharmacology, Cardiovascular Research Institute Maastricht, University of Maastricht, 6200 MD Maastricht, The Netherlands; and Departments of 2 Cardiothoracic Surgery and 4 Cardiology, Medical University of South Carolina, Charleston, South Carolina 29425 Recent...
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Published in | American journal of physiology. Heart and circulatory physiology Vol. 284; no. 1; pp. H364 - H371 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.01.2003
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Subjects | |
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Abstract | Departments of 1 Pathology and
3 Pharmacology, Cardiovascular Research Institute
Maastricht, University of Maastricht, 6200 MD Maastricht, The
Netherlands; and Departments of
2 Cardiothoracic Surgery and
4 Cardiology, Medical University of South Carolina,
Charleston, South Carolina 29425
Recent studies have been directed at
modulating the heart failure process through inhibition of activated
matrix metalloproteinases (MMPs). We hypothesized that a loss of MMP
inhibitory control by tissue inhibitor of MMP (TIMP)-1 deficiency
alters the course of postinfarction chamber remodeling and induced
chronic myocardial infarction (MI) in wild-type (WT) and
TIMP-1 / mice. Left ventricular (LV) pressure-volume
loops obtained from WT and TIMP-1 / mice demonstrated
that LV end-diastolic volume [52 ± 4 (WT) vs. 71 ± 6 (TIMP-1 / ) µl] and LV end-diastolic pressure
[9.0 ± 1.2 (WT) vs. 12.7 ± 1.4 (TIMP-1 / )
mmHg] were significantly increased in the TIMP-1 / mice
2 wk after MI. LV contractility was reduced to a similar degree in the
WT and TIMP-1 / groups after MI, as indicated by a
significant fall in the LV end-systolic pressure-volume relationship.
Ventricular weight and cross-sectional areas of LV myocytes were
significantly increased in TIMP-1 / mice, indicating
that the hypertrophic response was more pronounced. The observed
significant loss of fibrillar collagen in the TIMP-1 /
controls may have been an important contributory factor for the observed LV alterations in the TIMP-1 / mice after MI.
These findings demonstrate that TIMP-1 deficiency amplifies adverse LV
remodeling after MI in mice and emphasizes the importance of local
endogenous control of cardiac MMP activity by TIMP-1.
myocardial remodeling; pressure-volume loops |
---|---|
AbstractList | Recent studies have been directed at modulating the heart failure process through inhibition of activated matrix metalloproteinases (MMPs). We hypothesized that a loss of MMP inhibitory control by tissue inhibitor of MMP (TIMP)-1 deficiency alters the course of postinfarction chamber remodeling and induced chronic myocardial infarction (MI) in wild-type (WT) and TIMP-1
−/−
mice. Left ventricular (LV) pressure-volume loops obtained from WT and TIMP-1
−/−
mice demonstrated that LV end-diastolic volume [52 ± 4 (WT) vs. 71 ± 6 (TIMP-1
−/−
) μl] and LV end-diastolic pressure [9.0 ± 1.2 (WT) vs. 12.7 ± 1.4 (TIMP-1
−/−
) mmHg] were significantly increased in the TIMP-1
−/−
mice 2 wk after MI. LV contractility was reduced to a similar degree in the WT and TIMP-1
−/−
groups after MI, as indicated by a significant fall in the LV end-systolic pressure-volume relationship. Ventricular weight and cross-sectional areas of LV myocytes were significantly increased in TIMP-1
−/−
mice, indicating that the hypertrophic response was more pronounced. The observed significant loss of fibrillar collagen in the TIMP-1
−/−
controls may have been an important contributory factor for the observed LV alterations in the TIMP-1
−/−
mice after MI. These findings demonstrate that TIMP-1 deficiency amplifies adverse LV remodeling after MI in mice and emphasizes the importance of local endogenous control of cardiac MMP activity by TIMP-1. Recent studies have been directed at modulating the heart failure process through inhibition of activated matrix metalloproteinases (MMPs). We hypothesized that a loss of MMP inhibitory control by tissue inhibitor of MMP (TIMP)-1 deficiency alters the course of postinfarction chamber remodeling and induced chronic myocardial infarction (MI) in wild-type (WT) and TIMP-1(-/-) mice. Left ventricular (LV) pressure-volume loops obtained from WT and TIMP-1(-/-) mice demonstrated that LV end-diastolic volume [52 +/- 4 (WT) vs. 71 +/- 6 (TIMP-1(-/-)) microl] and LV end-diastolic pressure [9.0 +/- 1.2 (WT) vs. 12.7 +/- 1.4 (TIMP-1(-/-)) mmHg] were significantly increased in the TIMP-1(-/-) mice 2 wk after MI. LV contractility was reduced to a similar degree in the WT and TIMP-1(-/-) groups after MI, as indicated by a significant fall in the LV end-systolic pressure-volume relationship. Ventricular weight and cross-sectional areas of LV myocytes were significantly increased in TIMP-1(-/-) mice, indicating that the hypertrophic response was more pronounced. The observed significant loss of fibrillar collagen in the TIMP-1(-/-) controls may have been an important contributory factor for the observed LV alterations in the TIMP-1(-/-) mice after MI. These findings demonstrate that TIMP-1 deficiency amplifies adverse LV remodeling after MI in mice and emphasizes the importance of local endogenous control of cardiac MMP activity by TIMP-1. Departments of 1 Pathology and 3 Pharmacology, Cardiovascular Research Institute Maastricht, University of Maastricht, 6200 MD Maastricht, The Netherlands; and Departments of 2 Cardiothoracic Surgery and 4 Cardiology, Medical University of South Carolina, Charleston, South Carolina 29425 Recent studies have been directed at modulating the heart failure process through inhibition of activated matrix metalloproteinases (MMPs). We hypothesized that a loss of MMP inhibitory control by tissue inhibitor of MMP (TIMP)-1 deficiency alters the course of postinfarction chamber remodeling and induced chronic myocardial infarction (MI) in wild-type (WT) and TIMP-1 / mice. Left ventricular (LV) pressure-volume loops obtained from WT and TIMP-1 / mice demonstrated that LV end-diastolic volume [52 ± 4 (WT) vs. 71 ± 6 (TIMP-1 / ) µl] and LV end-diastolic pressure [9.0 ± 1.2 (WT) vs. 12.7 ± 1.4 (TIMP-1 / ) mmHg] were significantly increased in the TIMP-1 / mice 2 wk after MI. LV contractility was reduced to a similar degree in the WT and TIMP-1 / groups after MI, as indicated by a significant fall in the LV end-systolic pressure-volume relationship. Ventricular weight and cross-sectional areas of LV myocytes were significantly increased in TIMP-1 / mice, indicating that the hypertrophic response was more pronounced. The observed significant loss of fibrillar collagen in the TIMP-1 / controls may have been an important contributory factor for the observed LV alterations in the TIMP-1 / mice after MI. These findings demonstrate that TIMP-1 deficiency amplifies adverse LV remodeling after MI in mice and emphasizes the importance of local endogenous control of cardiac MMP activity by TIMP-1. myocardial remodeling; pressure-volume loops |
Author | Spinale, Francis G Hauet, Anne M Cleutjens, Jack P. M Daemen, Mat J. A. P Creemers, Esther E. J. M Hapke, Elizabeth Smits, Jos F. M Leenders, Peter Dowdy, Kathryn B Escobar, Patricia G Zile, Michael R Davis, Jeniffer N Parkhurst, Andrea M |
Author_xml | – sequence: 1 fullname: Creemers, Esther E. J. M – sequence: 2 fullname: Davis, Jeniffer N – sequence: 3 fullname: Parkhurst, Andrea M – sequence: 4 fullname: Leenders, Peter – sequence: 5 fullname: Dowdy, Kathryn B – sequence: 6 fullname: Hapke, Elizabeth – sequence: 7 fullname: Hauet, Anne M – sequence: 8 fullname: Escobar, Patricia G – sequence: 9 fullname: Cleutjens, Jack P. M – sequence: 10 fullname: Smits, Jos F. M – sequence: 11 fullname: Daemen, Mat J. A. P – sequence: 12 fullname: Zile, Michael R – sequence: 13 fullname: Spinale, Francis G |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/12388239$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1161/hc0702.104164 10.1095/biolreprod59.2.364 10.1016/S0008-6363(00)00003-1 10.1161/01.RES.85.4.364 10.1172/JCI8040 10.1161/hh1101.091862 10.1161/hc3401.093154 10.1152/ajpheart.2000.279.3.H1411 10.1152/ajpheart.1998.274.4.H1416 10.1016/S0022-2828(05)82390-9 10.1161/01.CIR.97.17.1708 10.1152/ajpheart.2000.278.1.H151 10.1161/01.CIR.84.5.2123 10.1038/13459 10.1152/ajpheart.2000.279.1.H443 10.1006/jmcc.1999.1052 10.1016/S0002-9440(10)65060-2 10.1161/hc0602.103674 10.1161/01.RES.76.5.907 10.1016/0022-1759(94)90005-1 10.1161/01.CIR.98.17.1728 10.1006/jmcc.2000.1294 10.1016/S0008-6363(98)00216-8 10.1161/hc3601.094298 10.1016/S0008-6363(00)00029-8 10.1172/JCI8768 10.1161/01.RES.82.4.482 10.1016/0014-5793(92)80015-9 10.1161/01.RES.67.1.23 10.1161/hh1501.094396 10.1152/ajpheart.1999.277.5.H1906 10.1161/01.CIR.99.23.3063 10.1006/jmcc.1998.0711 10.1006/jsre.1998.5330 |
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References | B20 B21 B22 B23 B24 B25 B27 B28 B29 B30 B31 B10 B32 B11 B33 B12 B34 B13 Robinson TF (B26) 1983; 49 B35 B14 B36 B15 B16 B17 B18 B19 B1 B3 B4 B5 B6 B7 B8 B9 Caulfield JB (B2) 1979; 40 |
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Snippet | Departments of 1 Pathology and
3 Pharmacology, Cardiovascular Research Institute
Maastricht, University of Maastricht, 6200 MD Maastricht, The
Netherlands;... Recent studies have been directed at modulating the heart failure process through inhibition of activated matrix metalloproteinases (MMPs). We hypothesized... |
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SubjectTerms | Animals Echocardiography Mice Mice, Knockout - genetics Myocardial Infarction - physiopathology Space life sciences Tissue Inhibitor of Metalloproteinase-1 - deficiency Tissue Inhibitor of Metalloproteinase-1 - genetics Ventricular Function, Left Ventricular Remodeling - physiology |
Title | Deficiency of TIMP-1 exacerbates LV remodeling after myocardial infarction in mice |
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