Metalloproteinases in metabolic syndrome

Berg, Gabriela; Miksztowicz, Verónica; Schreier, Laura

doi:10.1016/j.cca.2011.06.013

Cited by 49 publications

(56 citation statements)

References 99 publications

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“…Pro-MMP-9 requires a proteolytic process to become active and this activation is tightly regulated at the transcription level, at precursor zymogens activation, through interaction with specific ECM components, and by inhibition of endogenous inhibitors. Therefore, applied methods (mRNA synthesis, protein expression, and enzyme activity) and technical limitations (e.g., inability to differentiate between active and pro-enzymes by some antibodies) to evaluate MMPs should be considered when comparing the results of surveys [2,36]. [1] in the x-axis and t [2] in the y-axis, respectively) are shown.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, applied methods (mRNA synthesis, protein expression, and enzyme activity) and technical limitations (e.g., inability to differentiate between active and pro-enzymes by some antibodies) to evaluate MMPs should be considered when comparing the results of surveys [2,36]. [1] in the x-axis and t [2] in the y-axis, respectively) are shown. Individual associations of MMP-8 with obesity and hs-CRP may suggest higher MMP-8 in MetS systemic inflammation, probably originates from excessive adipose tissue [37].…”

Section: Discussionmentioning

confidence: 99%

“…Endothelial dysfunction in metabolic syndrome (MetS) patients renders them susceptible for developing cardiovascular disease (CVD) [1,2]. Circulating pro-inflammatory cytokines in their vascular tissues [3] mediate nuclear factor-kB (NF-κB) pathway activation [4] that contributes to a low-grade systemic inflammation associated with atherosclerosis and increased insulin resistance (IR) as important keys to MetS pathophysiology [5].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Evaluation of plasma MMP-8, MMP-9 and TIMP-1 identifies candidate cardiometabolic risk marker in metabolic syndrome: results from double-blinded nested case–control study

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Evaluation of plasma MMP-8, MMP-9 and TIMP-1 identifies candidate cardiometabolic risk marker in metabolic syndrome: results from double-blinded nested case–control study

et al. 2015

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“…The expression level of MMPs correlates with the invasion of cancer cells because the degradation of the ECM is essential for tumor angiogenesis, invasion, and metastasis (Gladson 1999;Shao et al 2011;Li et al 2011;Lee et al 2011). Amongst many MMPs that have been identified, MMP-2 (gelatinase-A) and MMP-9 (gelatinase-B) have been hypothesized to be key enzymes as they degrade type IV collagen (the main component of ECM) Ranogajec et al 2011;Berg et al 2011). Specifically, MMP-2 is up-regulated in gliomas and related cancers, but its expression level is trivial in normal brain tissue (Deshane et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Mutations in isocitrate dehydrogenase 2 accelerate glioma cell migration via matrix metalloproteinase-2 and 9

Zheng

et al. 2011

Biotechnol Lett

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The gene encoding isocitrate dehydrogenase (IDH) is somatically mutated predominantly in secondary glioblastoma multiforme. Glioma-specific mutations in IDH1 always produced a single amino acid substitution at R132, but mutations in IDH2 were exclusively at R172 which was the analogous site to R132 in IDH1. Mutations of IDH1 and IDH2 led to simultaneous loss and gain of activities in the production of α-ketoglutarate and 2-hydroxyglutarate, respectively. Matrix metalloproteinases (MMPs) are zinc-dependent endoproteinases involved in the degradation of the extracellular matrix. The exact role of IDH2 mutant on MMPs activity and cell migration has not been fully studied. Here, we show that in response to IDH2 mutations, low levels of α-ketoglutarate increased the stabilization of HIF-1α which can contribute to tumor growth. Moreover, mutant IDH2-induced HIF-1α improved the secretion levels of pro-MMP-2 and pro-MMP-9 as well as the conversion from pro-MMP-2 to its active form, giving C6 glioma cells a higher migration potential. The HIF-1α pathway is probably a critical pathway for release of MMPs in the glioma cancer harboring IDH mutant.

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“…Matrix metalloproteinase (MMP) is a family of zinc-dependent endopeptidase which is capable of destroying all components of the ECM. Matrix metalloproteinase-9 (MMP-9), also known as Gelatinase B or 92 kDa type IV collagenase, plays important roles in the pathogenesis of hypertension (Humphrey 2008;Berg et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Is there any genetic predisposition of MMP-9 gene C1562T and MTHFR gene C677T polymorphisms with essential hypertension?

et al. 2013

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The current study was conducted to determine whether there is a relation between hypertension and two different polymorphisms, including C1562T of the Matrix metalloproteinase-9 (MMP-9) gene and C677T of the methylenetetrahydrofolate reductase (MTHFR) gene. Genomic DNA obtained from 224 persons (125 patients with hypertension and 99 healthy controls) were used in the study. Polymorphisms were determined by using polymerase chain reaction-restriction fragment length polymorphism and electrophoresis. The results were statistically analyzed and were found to be statistically significant. The frequencies of the C1562T genotypes were found to be, in controls CC 75.8 % and CT 24.2 % and in patients CC 71.2 %, and CT 28.8 %. The frequencies of C677T genotype were found to be, in controls CC 56.6 %, CT 38.4 and TT 5.1 % in controls and in patients CC 52 %, CT 30.4 % and TT 17.6 %. In conclusion, we may suggest that there is no relation between the essential hypertension and C1562T polymorphism of MMP-9 gene; on the other hand C677T polymorphism (genotype TT) of MTHFR gene can be regarded as a genetic indicator for the development of essential hypertension.

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Metalloproteinases in metabolic syndrome

Cited by 49 publications

References 99 publications

Evaluation of plasma MMP-8, MMP-9 and TIMP-1 identifies candidate cardiometabolic risk marker in metabolic syndrome: results from double-blinded nested case–control study

Evaluation of plasma MMP-8, MMP-9 and TIMP-1 identifies candidate cardiometabolic risk marker in metabolic syndrome: results from double-blinded nested case–control study

Mutations in isocitrate dehydrogenase 2 accelerate glioma cell migration via matrix metalloproteinase-2 and 9

Is there any genetic predisposition of MMP-9 gene C1562T and MTHFR gene C677T polymorphisms with essential hypertension?

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