Differential Expression of MMPs and TIMPs in Moderate and Severe Heart Failure in a Transgenic Model

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

“…We observed increased mRNS levels in case of two matrix metalloproteinase genes; mmp2 and mmp9. Matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9) are increased in the rat brain after experimental ischemic stroke and they also contribute to myocardial remodeling after myocardial infarction (Machado et al, 2006;Mori, Gibson, & McTiernan, 2006) as well as in the development of acute infarction (Giricz et al, 2006). In our study these genes exhibited almost the most pronounced over-expressions due to perfusion.…”

“…Circulating levels of MMPs and TIMPs could reflect the atherosclerotic process occurring within the arterial wall and have been identified in normal and failing myocardium (Spinale, 2002). Recent studies suggest that MMPs and TIMPs play a role in various cardiovascular diseases including atherosclerosis and ventricular remodeling observed in heart failure (Mori et al, 2006).…”

Loss of Timp3 Gene Leads to Abdominal Aortic Aneurysm Formation in Response to Angiotensin II

“…A Coomassie Bluestained SDS-PAGE gel (after proteins were transferred to PVDF membrane) was used as a loading control. In situ gelatin zymography was performed on 14-m cryosections as described (31). Total collagenase and gelatinase activities were measured using Enzchek collagenase (catalog number D-12060) and elastase (catalog number E-12056) activity assay kits (from Millipore) as before (30).…”

Matrix metalloproteinase-1, -3, and -9 gene polymorphisms and the risk of idiopathic dilated cardiomyopathy in a Chinese Han population

“…Moreover, MMP-3 can participate in the activation cascade required to achieve activation of MMP species relevant to the LV remodeling process. The increased MMP-3 expression that occurred in DCM may be an important contributory mechanism for the LV remodeling in this form of heart failure [2][3][4][5][6]. A single adenine insertion/deletion polymorphism (5A/6A) at the − 1171 position of the MMP-3 promoter causes the elevation of transcriptional level and local expression of MMP-3.…”

“…The stromelysins, such as MMP-3, are of particular interest for its broad substrate portfolio and ability to activate other MMPs. The gelatinases, such as MMP-9, have been extensively studied because they are amenable to a number of in vitro measurement approaches [2][3][4][5][6]. The MMPs are regulated at various levels, and the transcription of MMPs is under tight control.…”