scholarly journals Some indicators of left ventricular dysfunction in hypertensive patients, depending on the level of matrix metalloproteinases and tissue inhibitors of metalloproteinase-1

2021 ◽  
Vol 102 (6) ◽  
pp. 815-820
Author(s):  
T V Kalinkina ◽  
N V Lareva ◽  
M V Chistyakova
Keyword(s):  
Matrix Metalloproteinases ◽  
Matrix Metalloproteinase ◽  
Diastolic Dysfunction ◽  
Longitudinal Strain ◽  
Global Longitudinal Strain ◽  
Serum Levels ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor

Aim. To study the level of matrix metalloproteinases-1 and -2, and tissue inhibitor of metalloproteinases-1, the indicator of left ventricular myocardial deformation in patients with stage 12 hypertension. Methods. 114 patients (40 women and 74 men) with hypertension of 12 stages observed in the cardiology Department of the Road clinical hospital Chita II were examined. The median age was 428.3 years. Left ventriclular diastolic function was studied by using tissue Doppler imaging in apical four-chamber views. Serum matrix metalloproteinase-1, matrix metalloproteinase-2, and tissue inhibitor of metalloproteinases-1 levels were measured in all patients on automated immunoassay analyzers using ready-to-use ELISA kits. Results. An increase in serum levels of matrix metalloproteinases-1 and -2 in the group of patients with hypertension and diastolic dysfunction by 46 and 47%, respectively, was found against increased levels of serum tissue inhibitor of metalloproteinase-1 (р=0.049). In patients with diastole dysfunction, myocardial global longitudinal strain was decreased in was observed by 22.8% compared with patients without diastole dysfunction (p 0.05). The analysis revealed a moderate negative relationship between left ventricular global longitudinal strain and the serum levels of metalloproteinases-2 (r=0.64, p 0.05). Conclusion. In patients with hypertension and left ventricular diastolic dysfunction, a decrease in left ventricular global longitudinal strain is associated with the serum level of matrix metalloproteinase-2; a tissue inhibitor of metalloproteinases-1 is unrelated to left ventricular global myocardial strain.

scholarly journals Plasma profiling determinants of matrix homeostasis in paediatric dilated cardiomyopathy

2010 ◽  
Vol 21 (1) ◽  
pp. 52-61 ◽  
Author(s):  
Tain-Yen Hsia ◽  
Jeremy M. Ringewald ◽  
Robert E. Stroud ◽  
Nadia Roessler ◽  
Nidhi Kumar ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Matrix Metalloproteinase ◽  
Dilated Cardiomyopathy ◽  
Plasma Levels ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Matrix Metalloproteinase 2 ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Tissue Inhibitors ◽  
Tissue Inhibitors Of Metalloproteinase

AbstractObjectiveDilated cardiomyopathy is an important cause of cardiac failure in both children and adults, but is more progressive in children. In adult dilated cardiomyopathy, left ventricular remodelling is associated with changes in the plasma levels of matrix metalloproteinases and tissue inhibitor of metalloproteinases. Plasma matrix metalloproteinases and tissue inhibitors of metalloproteinase changes in paediatric dilated cardiomyopathy have not been examined. This study developed a low blood volume, high-sensitivity assay to test the hypothesis that unique and differential plasma matrix metalloproteinases and tissue inhibitors of metalloproteinase profile exist in patients with paediatric dilated cardiomyopathy.Methods/resultsA systemic blood sample (1 millilitre) was obtained from seven children aged 8 plus or minus 7 years with dilated cardiomyopathy and 26 age-matched normal volunteers. Using a high-throughput multiplex suspension immunoassay, plasma levels were quantified for collagenases (matrix metalloproteinase-8), gelatinases (matrix metalloproteinase-2 and -9), lysins (matrix metalloproteinase-3 and -7), and tissue inhibitor of metalloproteinases-1, -2, and -4. The matrix metalloproteinase to tissue inhibitors of metalloproteinases ratios were also calculated. The plasma matrix metalloproteinase-2, -7, -8, and -9 levels were increased by greater than twofold in patients with dilated cardiomyopathy than normal patients (with p less than 0.05). Patients with dilated cardiomyopathy also had significantly higher tissue inhibitors of metalloproteinases-1 and -4 (298% and 230%; with p less than 0.05).ConclusionsThese unique findings show that a specific plasma matrix metalloproteinase/tissue inhibitor of metalloproteinase profile occurs in paediatric dilated cardiomyopathy when compared to the cases of normal children. These distinct differences in the determinants of myocardial matrix structure and function may contribute to the natural history of dilated cardiomyopathy in children and may provide a novel biomarker platform in paediatric dilated cardiomyopathy.

scholarly journals Steps involved in activation of the complex of pro-matrix metalloproteinase 2 (progelatinase A) and tissue inhibitor of metalloproteinases (TIMP)-2 by 4-aminophenylmercuric acetate

1995 ◽  
Vol 308 (2) ◽  
pp. 645-651 ◽  
Author(s):  
Y Itoh ◽  
S Binner ◽  
H Nagase
Keyword(s):  
Matrix Metalloproteinase ◽  
Noncovalent Complex ◽  
The Other ◽  
Gelatinolytic Activity ◽  
Matrix Metalloproteinase 2 ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Sh Group ◽  
Inhibitory Domain ◽  
Interstitial Collagenase

Tissue inhibitor of metalloproteinases (TIMP)-2 forms a noncovalent complex with the precursor of matrix metalloproteinase 2 (proMMP-2, progelatinase A) through interaction of the C-terminal domain of each molecule. We have isolated the proMMP-2-TIMP-2 complex from the medium of human uterine cervical fibroblasts and investigated the processes involved in its activation by 4-aminophenylmercuric acetate (APMA). The treatment of the complex with APMA-activated proMMP-2 by disrupting the Cys73-Zn2+ interaction of the zymogen. This is triggered by perturbation of the proMMP-2 molecule, but not by the reaction of the SH group of Cys73 with APMA. The ‘activated’ proMMP-2 (proMMP-2*) formed a new complex with TIMP-2 by binding to the N-terminal inhibitory domain of the inhibitor without processing the propeptide. Thus the APMA-treated proMMP-2*-TIMP-2 complex exhibited no gelatinolytic activity. In the presence of a small amount of free MMP-2, however, proMMP-2* in the complex was converted into the 65 kDa MMP-2 by proteolytic attack of MMP-2, but the complex did not exhibit gelatinolytic activity. The gelatinolytic activity detected after APMA treatment was solely derived from the activation of free proMMP-2. The removal of the propeptide of the proMMP-2* bound to TIMP-2 was also observed by MMP-3 (stromelysin 1), but not by MMP-1 (interstitial collagenase). MMP-3 cleaved the Asn80-Tyr81 bond of proMMP-2*. On the other hand, when MMP-3 was incubated with the proMMP-2-TIMP-2 complex, it bound to TIMP-2 and rendered proMMP-2 readily activatable by APMA. These results indicate that the blockage of TIMP-2 of the complex with an active MMP is essential for the activation of proMMP-2 when it is complexed with TIMP-2.

scholarly journals Contribution of Global and Regional Longitudinal Strain for Clinical Assessment of HFpEF in Coronary and Hypertensive Patients

Medicina ◽  
2021 ◽  
Vol 57 (12) ◽  
pp. 1372
Author(s):  
Gheorghe Stoichescu-Hogea ◽  
Florina Nicoleta Buleu ◽  
Ruxandra Christodorescu ◽  
Raluca Sosdean ◽  
Anca Tudor ◽  
...  
Keyword(s):  
Diastolic Dysfunction ◽  
Clinical Assessment ◽  
Longitudinal Strain ◽  
Systolic Dysfunction ◽  
Global Longitudinal Strain ◽  
Left Ventricular ◽  
Control Group ◽  
Hypertensive Patients ◽  
Group 2 ◽  
Artery Disease

Background: Contribution of global and regional longitudinal strain (GLS) for clinical assessment of patients with heart failure with preserved ejection fraction (HFpEF) is not well established. We sought to evaluate subclinical left ventricular dysfunction secondary to coronary artery disease (CAD) in HFpEF patients compared with hypertensive patients and age-matched healthy subjects. Material and methods: This was a retrospective study that included 148 patients (group 1 = 62 patients with HFpEF, group 2 = 46 hypertensive patients, and group 3 = 40 age-matched control subjects). Peak systolic segmental, regional (basal, mid, and apical), and global longitudinal strain were assessed for each study group using two-dimensional speckle-tracking echocardiography (2D-STE). Results: GLS values presented statistically significant differences between the three groups (p < 0.001); markedly increased values (more negative) were observed in the control group (−20.2 ± 1.4%) compared with HTN group values (−18.4 ± 3.0%, p = 0.031) and with HFpEF group values (−17.6 ± 2.3%, p < 0.001). The correlation between GLS values and HTN stages was significant, direct, and average (Spearman coefficient rho = 0.423, p < 0.001). GLS had the greatest ability to detect patients with HFpEF when HFpEF + CAD + HTN diastolic dysfunction (n = 30) + CON diastolic dysfunction (n = 2) from HFpEF + CAD + HTN + CON was analyzed. (optimal GLS limit of −19.35%, area under curve = 0.833, p < 0.001). Conclusions: Global longitudinal strain can be used for clinical assessment in differentiating coronary and hypertensive patients at higher risk for development of systolic dysfunction.

Reduction in levels of matrix metalloproteinases and increased expression of tissue inhibitor of metalloproteinase—2 in response to mild hypothermia therapy in experimental stroke

2005 ◽  
Vol 103 (2) ◽  
pp. 289-297 ◽  
Author(s):  
Jong Eun Lee ◽  
Yone Jung Yoon ◽  
Michael E. Moseley ◽  
Midori A. Yenari
Keyword(s):  
Matrix Metalloproteinases ◽  
Matrix Metalloproteinase ◽  
Mild Hypothermia ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Experimental Stroke ◽  
Tissue Inhibitor ◽  
Content Type ◽  
The Brain ◽  
Fine Print

Object. Mild hypothermia is a robust neuroprotectant, and the results of prospective clinical trials have indicated that it may improve neurological outcome in certain instances. One aspect of this protection has been associated with the prevention of blood—brain barrier (BBB) disruption. Matrix metalloproteinases (MMPs) have been implicated in BBB disruption because they can degrade the extracellular matrix. In this study the authors explored the relationship between hypothermia and MMPs and whether BBB preservation resulting from mild hypothermia therapy is due to alterations in MMP expression. Methods. Rats were subjected to middle cerebral artery occlusion for 2 hours; the animals were maintained in a state of normothermia or mild hypothermia (33°C) immediately after the onset of ischemia. The animals' brains were collected 2, 6, and 24 hours after ischemia began. Contrast-enhanced T1-weighted magnetic resonance imaging was performed at 24 hours to assess the extent of BBB disruption. Consistent with prior reports, areas of BBB disruption detected on T1-weighted images were smaller in the brains of rats maintained in a state of hypothermia (normothermia group 8.6 ± 3% of the brain; hypothermia group 0.2 ± 0.1% of the brain; p < 0.01). Expression of both MMP-2 and MMP-9 at the transcriptional and translational levels was reduced in hypothermic brains at 6 hours and 24 hours after ischemic injury. Matrix metalloproteinase—9 was primarily localized to cells of monocytic origin but was also observed in neurons and astrocytes. Matrix metalloproteinase—2 was found in some neurons and astrocytes but not in inflammatory cells. In addition, hypothermia increased the levels of the endogenous MMP inhibitor, tissue inhibitor of metalloproteinases—2. Conclusions. The authors conclude that mild hypothermia attenuates BBB disruption, decreases MMP expression, and suppresses MMP activity.

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