Matrix metalloproteinase-9 (MMP-9), a key determinant of extracellular matrix degradation, might cause cerebral damage after stroke and be involved in the development of depressive symptoms.
MMP-9 polymorphisms were independently associated with severe stroke and higher risk of END, and prestroke antithrombotic treatment was associated with less severe stroke and lower risk of END in patients with AF.
The present study is the first to demonstrate that cold exposure exacerbates imbalance between MMP-9 and TIMP-1 by activating the RAS, which may be critical in the initiation of stroke during chronic hypertension.
Impact statement Matrix metalloproteinase-9 ( MMP-9) is a possible candidate gene for some diseases, including metabolic syndrome, stroke, coronary artery disease (CAD).
Compared with this, 11 genetic factors such as MMP9 were found to be differentially expressed in both acute and recovery phases of stroke showing their indicating roles in stroke.
S1RA-treated mice showed faster behavioural recovery from stroke; this finding complements the significant decreases in matrix metalloproteinase-9 (MMP-9) expression and reactive astrogliosis surrounding the infarcted cortex.
Using our polymeric system to deliver VEGF-A and MMP-9, we improved recovery after stroke to an equivalent degree as observed with traditional stem cell treatment in a rodent model.
There was a robust increase in MMP-9 expression (immunofluorescence) in the ischemic vs. the non-ischemic hemisphere of MMP-9<sup>+/+</sup> but not MMP-9<sup>-/-</sup> mice, 24 h after stroke.
Plasma MMP-9 concentrations were determined using enzyme-linked immunosorbent assay, and sHT was diagnosed based on brain computed tomography or magnetic resonance performed 3-14 d after stroke onset.
Diagnostic accuracy of a single measurement of the 3 biomarkers for stroke using AUC (95% confidence interval) plots were as follows: .84 (.77-0.91), P < .0001, for GFAP; .85 (.79-0.92), P < .0001, for copeptin; and .65 (.56-0.73), P = .0003, for MMP-9.
An insignificant relationship between MMP-9 and clinical events within 1 year (death, AMI, or stroke) (n = 15) was observed, probably due to the lack of statistical power.
MMP-9 is involved in the pathological process of hemorrhagic stroke through a variety of mechanisms and is closely related to prognosis after cerebral hemorrhagic stroke.
Combination therapy also decreased BBB leakage (P<0.001), MMP-9 level or edema (P<0.05) and improved neurological functions at 24 and 48h after stroke.
Matrix metalloproteinases (MMPs), specifically MMP-2, MMP-7, and MMP-9, have been discovered to be linked to many forms of vascular diseases such as stroke, and their detection is crucial to facilitate clinical diagnosis.
Therefore, our findings demonstrate that miconazole protects blood vessels from hemorrhages by downregulating the pERK-MMP9 axis from zebrafish to mammals and shed light on the potential of phenotype-based screens in zebrafish for the discovery of new drug candidates and chemical probes for hemorrhagic stroke.
In conclusion, our findings suggest that MMP-9 C(-1562)T polymorphism is significantly associated with risk of stroke in patients with and without T2DM.