Role of mast cell chymase and tryptase in the progression of atherosclerosis: study in 44 autopsied cases

Ramalho, Luciana Santos; Oliveira, Lívia Ferreira; Cavellani, Camila Lourencini; Ferraz, Mara Lúcia da Fonseca; Oliveira, Flávia Aparecida de; Corrêa, Rosana Rosa Miranda; Teixeira, Vicente de Paula Antunes; Pereira, Sanívia Aparecida de Lima

doi:10.1016/j.anndiagpath.2012.04.007

Cited by 30 publications

(17 citation statements)

References 21 publications

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“…Moreover, both chymase and tryptase were shown to be positively correlated with the degree of atherosclerosis in human aortas (Ramalho et al, 2013). Tryptase is known to degrade ECM by activating pro-MMPs (Johnson et al, 1998) while also breaking down fibronectin (Mäyränpää et al, 2006).…”

Section: Mast Cell Mediated Atherosclerosis Progressionmentioning

confidence: 98%

The impact of mast cells on cardiovascular diseases

Kritikou

Kuiper

Kovanen

et al. 2016

European Journal of Pharmacology

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Section: Mast Cell Mediated Atherosclerosis Progressionmentioning

confidence: 98%

The impact of mast cells on cardiovascular diseases

Kritikou

Kuiper

Kovanen

et al. 2016

European Journal of Pharmacology

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“…17 In aortic atherosclerosis, immunostaining of aortic sections derived from autopsies of 44 patients (aged 36-69 years) with various degrees of atherosclerosis demonstrated that the levels of mast cell chymase and tryptase correlated positively with the levels of collagen and the extent of lipid deposition in the atherosclerotic lesions. 18 In a group of 65 patients with acute coronary syndromes, the levels of serum tryptase on hospital admission were found to be predictive of cardiovascular complexity, as defined by an angiographic scoring system (SYNTAX score), even more reliably than other biomarkers in use. 19 …”

Section: Reviewsmentioning

confidence: 98%

“…13 Importantly, in a 2013 autopsy study, the levels of aortic chymase and tryptase correlated with disease progression. 18 Chymase and tryptase not only induce apoptosis of various plaque cells, but can also directly or indirectly degrade extracellular matrix molecules, thereby reducing plaque integrity and/or stability. For example, chymase, tryptase, and cathep sin G can cleave vascular endothelial cadherin and fibronectin, which are necessary for endothelial cell adhesion, and thereby contribute to endothelial erosion.…”

Section: Protease Releasementioning

confidence: 99%

Mast cells in human and experimental cardiometabolic diseases

2015

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Mast cells, like many other types of inflammatory cell, perform pleiotropic roles in cardiometabolic diseases such as atherosclerosis, abdominal aortic aneurysms, obesity, and diabetes mellitus, as well as complications associated with these diseases. Low numbers of mast cells are present in the heart, aorta, and adipose tissue of healthy humans, but patients with cardiometabolic diseases and animals with experimentally-induced cardiometabolic pathologies have high numbers of mast cells with increased activity in the affected tissues. Mediators released by the activated mast cells, such as chemokines, cytokines, growth factors, heparin, histamine, and proteases, not only function as biomarkers of cardiometabolic diseases, but might also directly contribute to the pathogenesis of such diseases. Mast-cell mediators impede the functions of vascular cells, the integrity of the extracellular matrix, and the activity of other inflammatory cells, thereby contributing to the pathobiology of the conditions at multiple levels. In mouse models, mast-cell activation aggravates the progression of various cardiometabolic pathologies, whereas a genetic deficiency or pharmacological stabilization of mast cells, or depletion or inhibition of specific mast-cell mediators, tends to delay the progression of such conditions. Pharmacological inhibition of mast-cell activation or their targeted effector functions offers potential novel therapeutic strategies for patients with cardiometabolic disorders.

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“…17-20 Diyabetik nefropati 21 , renal fibrozis, 22-24 akciğer fibrozisi [25][26][27] , ateroskleroz 28,29 ve kanserlerde mast hücre sayısı artmaktadır. 13,30,31 HPS ile ilişkili mast hücrelerini değerlendiren çalışmalar az sayıdadır.…”

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