Although no association was found between the TIMP-2 (-418G/C) polymorphism and the acne vulgaris, patients with the MMP-2 CT/TIMP-2 GG or GC allele are at higher risk of acne vulgaris.
Although no association was found between the TIMP-2 (-418G/C) polymorphism and the acne vulgaris, patients with the MMP-2 CT/TIMP-2 GG or GC allele are at higher risk of acne vulgaris.
Infection of primary macrophages by chimeric HIV clones containing brain-derived envelope fragments from patients with HIV-associated dementia (HAD) or nondemented AIDS patients (HIV-ND) showed that MMP-2 and -9 levels in conditioned media were significantly higher for the HAD clones.
The mean serum matrix metalloproteinase-2 level was significantly higher in the active acromegaly patients than in the controlled acromegaly patients (150.1 ± 54.5 ng/mL vs. 100.2 ± 44.6 ng/mL; p < 0.0001).
Pooled analyses demonstrated no significant differences in MMP-1 (4 studies; P = 0.21), MMP-2 (5 studies; P = 0.62) and MMP-3 levels (2 studies; P = 0.94) between AAD patients and control subjects; and significantly higher MMP-8 (2 studies; SMD 2.11; P = 0.020), MMP-9 (9 studies; SMD 1.54; P < 0.001) and MMP-12 levels (2 studies; SMD 1.33; P < 0.001) in AAD patients than in control subjects.
The plasma level of MMP-2 in health controls was 34.9 ± 6.9 ng/mL, and that it significantly increased to 46.2 ± 13.2 ng/mL in ACS patients.MMP-2 is a target gene of miR-29b.
The obtained results permit to conclude that the increased expression of MMP-2 and MMP-9 metalloproteinases and their tissue inhibitor (TIMP-2) is responsible for disturbed equilibrium of the metalloproteinase/tissue inhibitors system and as a consequence, for destabilization of atherosclerotic plaque and occurrence of the acute coronary syndrome in the investigated group of patients.
In this study, we investigated the expression level of miR-29b and MMP-2 in acute coronary syndrome (ACS) patients, verified whether MMP-2 is the target gene of miR-29b by luciferase reporter gene system, and explored the role of miR-29b in the viability and apoptosis of SMCs.
MMP-9 and MMP-2 activity and expression were assessed in colonic mucosal specimens from 8 patients with acute ischemic colitis and in 12 controls with a normal colonoscopy.
Our findings suggest that the degradation of tight junction proteins ZO-1, claudin-5 and occludin by MMP-2 and -9 secreted by leukemic cells constitutes an important mechanism in the BBB breakdown which contributes to the invasion of leukemic cells to the CNS in acute leukemia.