scholarly journals The Role of Matrix Metalloproteinases in Endometriosis: A Potential Target

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1739
Author(s):  
Junya Ke ◽  
Jiangfeng Ye ◽  
Mingqing Li ◽  
Zhiling Zhu

Endometriosis is a condition that is influenced by hormones and involves stroma and glands being found outside the uterus; there are increases in proliferation, invasion, internal bleeding, and fibrosis. Matrix metalloproteinases (MMPs) have been suggested to be crucial in the progression of invasion. The MMP family includes calcium-dependent zinc-containing endopeptidases, some of which not only affect the process of cell invasion but also participate in other physiological and pathological processes, such as angiogenesis and fibrosis. MMPs act as downstream-targeted molecules and their expression can be regulated by numerous factors such as estrogen, oxidative stress, cytokines, and environmental contaminants. Given their unique roles in endometriosis, MMPs may become effective biomarkers of endometriosis in the future. In the present review, we summarize the current literature on MMPs regarding their classification, function, and potential value for endometriosis, which may contribute to our knowledge of MMPs and MMP-targeted interventions.

2007 ◽  
Vol 50 (2) ◽  
pp. 109-111 ◽  
Author(s):  
Anna Potáčová ◽  
Michaela Adamcová ◽  
Martin Štěrba ◽  
Olga Popelová ◽  
Tomáš Šimůnek ◽  
...  

Matrix metalloproteinases (MMPs), activated by oxidative stress, play a key role during cardiac remodeling. In the present study we aimed to assess the role of MMPs in experimental cardiomyopathy induced by repeated 10-week administration of daunorubicin (3 mg/kg i.v.) to rabbits. In the daunorubicin group, the plasma cardiac troponin T levels (cTnT – a marker of myocardial necrosis) were significantly increased (p<0.05), commencing with the 8th administration compared with the controls. The amount of collagen (an estimate of fibrosis) was also significantly higher in the daunorubicin group (13.39 ± 0.97 mg/g wet weight) compared to the control group (10.03 ± 0.65 mg/g wet weight). In both groups, the LV MMP-activity was observed only in the gelatine substrate in the 70 kDa region (MMP-2), while no MMPs activities were detectable either in the casein or collagen containing zymograms. At the end of the experiment, the MMP- 2 activity was slightly up-regulated (by 16 %) compared with the controls.


Biochimie ◽  
2005 ◽  
Vol 87 (3-4) ◽  
pp. 307-314 ◽  
Author(s):  
Uta B. Hofmann ◽  
Roland Houben ◽  
Eva-B. Bröcker ◽  
Jürgen C. Becker

Author(s):  
Dragana Stanisic ◽  
Radmila Obradovic ◽  
Sanja Vujovic ◽  
Milica Jovanovic ◽  
Vladimir Zivkovic

Abstract Diabetes mellitus, a chronic disease considered by the World Health Organization to be an epidemic, is now recognized as one of the factors behind the onset of periodontal disease. The connection between periodontal disease, which is an irreversible inflammatory disease of the supporting tissue of the teeth, and systemic diseases is reflected in the existence of common risk factors, subgingival dental biofilm, as a constant source of proinflamma-tory cytokines synthesized intensely in inflammatory periodontium. Diabetes mellitus leads to increased oxidative stress in periodontal tissues causing worsening of the disease and periodontopathy exacerbates deficiency of pancreatic β-cells. The most important role in primary inflammatory response in the pathogenesis of periodontopathy is played by neutrophils. Neutrophils cause periodontium destruction by the release of enzymes (matrix metalloproteinases), cytotoxic substances (free radicals, reactive oxygen and nitrogen species) and the expression of membrane receptors. Matrix metalloproteinases within the “protease network” are critical to many physiological and pathological processes, including immunity, inflammation, bone resorption and wound healing. Matrix metalloproteinases levels are elevated in patients with metabolic syndrome and diabetes mellitus, which may contribute to more frequent complications. In this paper, the review of available literature data shows the correlation between periodontal disease and diabetes mellitus, as well as the role of matrix metalloproteinases and oxidative stress in these. In this regard, determining the value of matrix metalloproteinases may be helpful in the diagnosis of periodontal disease complicated by diabetes mellitus. Also, the parameters of oxidative stress could help to clarify the mechanisms of pathogenesis and etiology of periodontal disease, or indicate the potential benefit of antioxidant supplementation in these individuals. As the role of matrix metalloproteinases has not been fully clarified in the pathogenesis of periodontopathy, additional studies will be needed to indicate their importance.


2019 ◽  
Vol 17 (3) ◽  
pp. 821-835 ◽  
Author(s):  
Victor Laurent ◽  
Aurélie Toulet ◽  
Camille Attané ◽  
Delphine Milhas ◽  
Stéphanie Dauvillier ◽  
...  

2020 ◽  
Vol 219 (8) ◽  
Author(s):  
Amita Arora ◽  
Vesa M. Olkkonen

Invadopodia are dynamic protrusions that harbor matrix metalloproteinases for pericellular matrix degradation. However, the mechanisms underlying their maturation are poorly understood. Pedersen et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.202003063) demonstrate a dual role of Protrudin in invadopodia elongation and matrix degradation, central to cell invasion and cancer metastasis.


2019 ◽  
Vol 316 (3) ◽  
pp. H647-H663 ◽  
Author(s):  
Mohamed M. Ali ◽  
Abeer M. Mahmoud ◽  
Elizabeth Le Master ◽  
Irena Levitan ◽  
Shane A. Phillips

The glycocalyx is crucial for normal endothelial function. It also tethers extracellular superoxide dismutase (SOD3), which protects the endothelium against oxidative damage. Proteolytic enzymes [matrix metalloproteinases (MMPs)] are capable of disrupting endothelial cell surface proteins, such as syndecans, resulting in derangements of the endothelial glycocalyx. We sought to test the role of MMPs in oxidative stress-mediated disruption of the endothelial glycocalyx and examine the effect of pharmacological inhibition of MMPs on mitigating this detrimental effect. We also examined the role of histone deacetylase (HDAC) in the oxidative stress-mediated MMP induction and glycocalyx remodeling. Oxidative stress was experimentally induced in human adipose microvascular endothelial cells using H2O2 and buthionine sulfoximine in the presence and absence of potent MMP and HDAC inhibitors. H2O2 and buthionine sulfoximine resulted in a notable loss of the endothelial glycocalyx; they also increased the expression and proteolytic activity of MMP-2 and MMP-9 and subsequently increased the shedding of syndecan-1 and SOD3 from the endothelial cell surface. MMP upregulation was accompanied by a decline in mRNA and protein levels of their inhibitors, tissue inhibitors of metalloproteinase (TIMPs; TIMP-1 and TIMP-3). Furthermore, oxidative stress induced HDAC activity. Inhibition of MMPs and HDAC reversed syndecan-1 and SOD3 shedding and maintained endothelial glycocalyx integrity. HDAC inhibition increased TIMP expression and reduced MMP expression and activity in endothelial cells. Our findings shed light on MMPs and HDAC as therapeutically targetable mechanisms in oxidative stress-induced glycocalyx remodeling. NEW & NOTEWORTHY Oxidative stress, a hallmark of many diseases, damages the endothelial glycocalyx, resulting in vascular dysfunction. Studying the mechanistic link between oxidative stress and endothelial glycocalyx derangements might help discover new therapeutic targets to preserve vascular function. In this study, we investigated the involvement of matrix metalloproteinases and histone deacetylase in oxidative stress-induced endothelial glycocalyx degradation.


2018 ◽  
Vol 12 (2) ◽  
pp. 55-61 ◽  
Author(s):  
A. N. Strizhakov ◽  
Е. V. Timokhina ◽  
S. M. Ibragimova ◽  
V. S. Belousova ◽  
Ya. O. Martirosyan

In the present review, a new approach to studying the pathogenesis and predicting the development of preeclampsia (PE) – namely, the determination of matrix metalloproteinases (MMPs) – is discussed. Currently, the major cause of PE is thought to be an incomplete remodeling of spiral arteries because of an insufficient number of invading cytotrophoblasts or the absence/inactivation of crucial lysing enzymes, i.e. matrix metalloproteinases. The role of MMP-1, MМP-2, MМP-3, MМP-7, MМP-9 in the placenta formation, the development of oxidative stress and endothelial dysfunction is described. We propose that in the future, the MMPs may be used for differentially predicting early and late PE.


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