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Case 3.11
Published in Monica Fawzy, Plastic Surgery Vivas for the FRCS(Plast), 2023
Matrix metalloproteinases are enzymes that degrade extracellular protein:their inhibition is implicated in excessive scarring, andtheir overstimulation is implicated in chronic wounds.
Cytokine Effects on Extracellular Matrix
Published in Jason Kelley, Cytokines of the Lung, 2022
Ganesh Raghu, Michael Kinsella
Modulation of the expression of the other metalloproteinases has been less studied. Stromelysin is induced by IL-1 (Murphy et al., 1986), TGF, and bFGF (Edwards et al., 1987). Induction of human 72-kd type IV collagenase is enhanced by cells treated with TGF-β (Collier et al. 1988). This is in contrast with the effect of TGF-β on interstitial collagenase, since TGF-β decreases its synthesis by fibroblasts (Overall et al., 1989). Expression of 92 kd type IV collagenase is induced by EGF and IL-1 (Wilhelm et al., 1989).
Gene Therapy for Cardiovascular Diseases
Published in Yashwant Pathak, Gene Delivery, 2022
Dhwani Thakkar, Vandit Shah, Jigna Shah
A thrombosis can be caused by a ruptured plaque in an atherosclerotic artery, resulting in an acute ischemic episode, such as unstable angina and myocardial infarction. Transfer of the tissue inhibitor of metalloproteinase (TIMP) gene can aid in the stabilization of unstable plaques.25 Many studies have shown that transferring genes for biological indicators, including hirudin, thrombodulin, tissue plasminogen activator, cyclooxygenase, and tissue factor pathway inhibitor, lowers thrombotic events.15
N-acetyl cysteine can blunt metabolic and cardiovascular effects via down-regulation of cardiotrophin-1 in rat model of fructose-induced metabolic syndrome
Published in Archives of Physiology and Biochemistry, 2023
Azza S. Abdelhaffez, Ebtihal A. Abd El-Aziz, Maha B. Tohamy, Asmaa M. Ahmed
In line with these reports, López-Andrés et al. (2012) verified that CT-1 treatment increased left ventricular volumes and induced myocardial dilatation and myocardial fibrosis meanwhile, in aorta, arterial stiffness, vascular media thickness, collagen, and fibronectin content were increased by CT-1 treatment. Also, it has been proposed that CT-1 accelerates the development of atherosclerotic lesions by stimulating the inflammasome, foam cell formation and collagen-1 production in vascular smooth muscle cells (Konii et al.2013). In addition, in an in vitro study, it was found that CT-1 induces the proteolytic potential in human aortic endothelial cells by up-regulating matrix metalloproteinase-1 expression thus, may play an important role in the pathophysiology of atherosclerosis and plaque instability (Tokito et al.2013). On the other hand, decreased arterial stiffness, media thickness and vascular wall fibrosis were demonstrated in CT-1-null mice (Lopez-Andres et al.2013).
Predictors of coronary artery calcification and its association with cardiovascular events in patients with chronic kidney disease
Published in Renal Failure, 2021
Xue-rong Wang, Liang- Yuan, Rui- Shi, Huan- Li, De-guang Wang, Yong-gui Wu
By binary logistic analysis, we demonstrated that NLR was significantly correlated with an increased risk for CAC. The mechanism by which the NLR results in an increased risk for CAC involves the fact that neutrophils can release a variety of inflammatory mediators and cytokines, thus leading to chronic microinflammation and deteriorating vascular calcification [16]. Moreover, neutrophils activate peroxidase and lead to increased production of oxygen free radicals. Second, the expression of matrix metalloproteinases becomes upregulated in these circumstances, which results in the degradation of extracellular matrix components, such as collagen fibers and elastic fibers. The degradation products can then accelerate vascular smooth muscle transdifferentiation into osteoblastic cells, thus contributing to vascular calcification. Third, lymphocyte apoptosis mediates the production of inflammatory mediators and accelerates vascular calcification [17].
Resveratrol inhibits ACHN cells via regulation of histone acetylation
Published in Pharmaceutical Biology, 2020
Lili Dai, Lingyan Chen, Wenjing Wang, Peizheng Lin
Matrix metalloproteinases are considered to be regulatory factors of tumour microenvironment and carcinogenesis (Strbac et al. 2018). The MMPs are involved in the key ECM degradation of proteolytic enzyme family (Curran et al. 2004; Chen KE et al. 2018; Qiao et al. 2018) and are used to disrupt the interaction of cells–cells and cells–ECM by tissue remodelling. Studies have shown that the MMPs, particularly MMP-2 and MMP-9, key members of the MMP family, play a vital role in angiogenesis, invasion and transferring of tumours, including RCC (Ramos et al. 2016; Chen et al. 2017; Liu et al. 2017; Beardo et al. 2019). Therefore, gelatine zymography was performed to determine the activity of MMP-2/-9. We found that resveratrol significantly decreased MMP-2 and MMP-9 expressions. However, one previous research reported that the expression level of MMP-2 in ACHN cells was not affected by resveratrol (Zhao et al. 2018). The difference may be explained by concentrations of resveratrol and action times applied in the two studies. These data indicated that resveratrol could inhibit activity of MMP-2/-9. Studies have shown that MMP-2/-9 activity is associated with histone acetylation (Yeh et al. 2016).