Circulating Tissue Inhibitor of Matrix Metalloproteinase‐4 (TIMP‐4) in Systemic Sclerosis Patients with Elevated Pulmonary Arterial Pressure
Author(s) -
Gialafos J. Elias,
Moyssakis Ioannis,
Psaltopoulou Theodora,
P. Dimitrios,
Perea Despoina,
Vlasis Kostantinos,
Kostopoulos Charalampos,
Votteas Vassilios,
Sfikakis P. Petros
Publication year - 2008
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2008/164134
Subject(s) - medicine , matrix metalloproteinase , fibrosis , tissue inhibitor of metalloproteinase , extracellular matrix , cardiology , pulmonary fibrosis , lung , pulmonary hypertension , pulmonary artery , pulmonary function testing , blood pressure , pathology , biology , microbiology and biotechnology
Decreased levels of matrix metalloproteinases (MMPs) or excess levels of their tissue inhibitors (TIMPs) may contribute to dysregulation of extracellular matrix turnover in systemic sclerosis (SSc). In a cross-sectional study of 106 SSc patients, we measured serum levels of TIMP-4 which is preferentially expressed in cardiovascular structures and searched for correlations with simultaneously performed echocardiography measurements of pulmonary artery systolic pressure (PASP), myocardial performance, and pulmonary function tests. TIMP-4, but not MMP-9, levels were significantly raised in patients with SSc than controls. However, in the subgroup of patients with PASP measurements lower to 40 mmHg ( n = 69), TIMP-4 levels were comparable to controls irrespective of the presence of diffuse or limited skin involvement, or lung fibrosis. Individual PASP measurements suggestive of pulmonary hypertension were associated with increased TIMP-4 serum levels ( P = .03), independently of age, extent of skin sclerosis, or lung fibrosis, suggesting a cardiopulmonary vasculature-specific role of TIMP-4 activation in SSc.
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