Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concurrence of acute coronary syndromes with allergic or hypersensitivity as well as with anaphylactic or anaphylactoid reactions is increasingly encountered in clinical practice and there are several reports associating mast cell activation with acute cardiovascular events in adults. It was first described by Kounis as "allergic angina syndrome" progressing to "allergic myocardial infarction". The main mechanism proposed is the vasospasm of coronary arteries. This condition has not been described in childhood. We present a 13-year-old boy, admitted to our hospital with thoracic pain, 30 min after the ingestion of an oral dose of 500 mg of amoxicillin/clavulanic acid.
Int J Cardiol 2009 Jul 24
PMID:Kounis syndrome secondary to amoxicillin/clavulanic acid use in a child. 1863 72

Heart failure (HF) is a chronic syndrome in which pathological cardiac remodeling is an integral part of the disease and mast cell (MC) degranulation-derived mediators have been suggested to play a role in its progression. Protein kinase C (PKC) signaling is a key event in the signal transduction pathway of MC degranulation. We recently found that inhibition of epsilonPKC slows down the progression of hypertension-induced HF in salt-sensitive Dahl rats fed a high-salt diet. We therefore determined whether epsilonPKC inhibition affects MC degranulation in this model. Six week-old male Dahl rats were fed with a high-salt diet to induce systemic hypertension, which resulted in concentric left ventricular hypertrophy at the age of 11 weeks, followed by myocardial dilatation and HF at the age of 17 weeks. We administered epsilonV1-2, an epsilonPKC-selective inhibitor peptide (3 mg/kg/day), deltaV1-1, a deltaPKC-selective inhibitor peptide (3 mg/kg/day), TAT (negative control; at equimolar concentration; 1.6 mg/kg/day) or olmesartan (angiotensin receptor blocker [ARB] as a positive control; 3 mg/kg/day) between 11 weeks and 17 weeks. Treatment with epsilonV1-2 attenuated cardiac MC degranulation without affecting MC density, myocardial fibrosis, microvessel patency, vascular thickening and cardiac inflammation in comparison to TAT- or deltaV1-1-treatment. Treatment with ARB also attenuated MC degranulation and cardiac remodeling, but to a lesser extent when compared to epsilonV1-2. Finally, epsilonV1-2 treatment inhibited MC degranulation in isolated peritoneal MCs. Together, our data suggest that epsilonPKC inhibition attenuates pathological remodeling in hypertension-induced HF, at least in part, by preventing cardiac MC degranulation.
J Mol Cell Cardiol 2008 Dec
PMID:Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure. 1880 78

Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.
Int J Cardiol 2010 Mar 04
PMID:Kounis syndrome: a manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material. 2054 82

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. We present a case of recurrent acute myocardial infarction associated with an allergic reaction in an 83-year-old Italian woman.
Int J Cardiol 2010 Jul 09
PMID:Recurrent acute myocardial infarction and Kounis syndrome. 1914 25

A sixty-one year old female with a past history of asthma was admitted to the emergency department because of vertigo, nausea, vomiting, chest pain and generalized erythema after taking an oral dose of cefuroxime axetil. Electrocardiography showed ST segment elevation in inferior leads. After coronary angiography, type 2 variant of Kounis Syndrome is diagnosed. We present first drug induced Kounis Syndrome in an asthmatic patient with severe anaphylactic shock. The present report also shows that atopic people expressing an amplified mast cell degranulation may have more serious hemodynamic decompensation during hypersensitivity reactions.
Int J Cardiol 2009 Nov 12
PMID:Kounis Syndrome secondary to cefuroxime axetil use in an asthmatic patient. 1942 33

Evaluation of: Sun J, Sukhova GK, Wolters PJ et al.: Mast cells promote atherosclerosis by releasing pro-inflammatory cytokines. Nat. Med. 13, 719-724 (2007). Mast cells are important components in human allergic response and innate immunity. These cells have been implicated in the pathogenesis of atherosclerosis since the 1950s, and a series of studies have proposed their roles in the pathologic events critical to atherogenesis. Despite these studies and hypotheses, there is no evidence to suggest a direct participation of these allergic cells in atherosclerosis. Using mast cell-deficient mice and intravenous mast cell reconstitution technology with a conventional mouse atherosclerosis model, Dr Sun et al. revealed that mast cells contribute to atherogenesis by releasing proinflammatory cytokines, which are utilized to stimulate vascular cell-protease expression and further tissue remodeling. Mice that lack these cells are resistant to diet-induced atherosclerosis. These data suggest that stabilization of mast cells with antiallergic medicine may be utilized in controlling or preventing the initiation and progression of atherosclerosis in humans.
Future Cardiol 2007 Nov
PMID:Management of atherosclerosis with antiallergic medicine: a lesson from the mouse model. 1980 80

The clinical outcome of cardiovascular diseases as myocardial infarction and stroke are generally caused by rupture of an atherosclerotic plaque. However, the actual cause of a plaque to rupture is not yet established. Interestingly, pathology studies have shown an increased presence of the mast cell, an important inflammatory effector cell in allergy and host defense, in (peri)vascular tissue during plaque progression, which may point towards a causal role for mast cells. Very recent data in mouse models show that mast cells and derived mediators indeed can profoundly impact plaque progression, plaque stability and acute cardiovascular syndromes such as vascular aneurysm or myocardial infarction. In this review, we discuss recent evidence on the role of mast cells in the progression of cardiovascular disorders and give insight in the therapeutic potential of modulation of mast cell function in these processes to improve the resilience of a plaque to rupture.
Curr Cardiol Rev 2008 Aug
PMID:Mast cells: pivotal players in cardiovascular diseases. 1993 93

Acute stretch caused by volume overload (VO) of aorto-caval fistula (ACF) induces a variety of myocardial responses including mast cell accumulation, matrix metalloproteinase (MMP) activation, and collagen degradation, all of which are critical in dictating long-term left ventricle (LV) outcome to VO. Meanwhile, these responses can be part of myocardial inflammation dictated by tumor necrosis factor-alpha (TNF-alpha), which is elevated after acute ACF. However, it is unknown whether TNF-alpha mediates a major myocardial inflammatory response to stretch in early VO. In 24-h ACF and sham rats, microarray gene expression profiling and subsequent Ingenuity Pathway Analysis identified a predominant inflammatory response and a gene network of biologically interactive genes strongly linked to TNF-alpha. Western blot demonstrated increased local production of TNF-alpha in the LV (1.71- and 1.66-fold in pro- and active-TNF-alpha over control, respectively, P<0.05) and cardiomyocytes (2- and 4-fold in pro- and active-TNF-alpha over control, respectively, P<0.05). TNF-alpha neutralization with infliximab (5.5 mg/kg) attenuated the myocardial inflammatory response to acute VO, as indicated by inhibition of inflammatory gene upregulation, myocardial infiltration (total CD45+ cells, mast cells, and neutrophils), MMP-2 activation, collagen degradation, and cardiac cell apoptosis, without improving LV remodeling and function. These results indicate that TNF-alpha produced by cardiomyocytes mediates a predominant inflammatory response to stretch in the early VO in the ACF rat, suggesting an important role of TNF-alpha in initiating pathophysiological response of myocardium to VO.
J Mol Cell Cardiol 2010 Jul
PMID:Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload. 2004 5

Although numerous reports support the existence of stem cells in the adult heart, few studies have been conducted using human cardiac tissue. Therefore, cells from human cardiac atrial biopsies were analyzed regarding progenitor properties. Expression of stem cell markers was analyzed using fluorescence-activated cell sorting. This identified a small population of C-kit+ cells, which could be further subdivided based on expression of CD45. The C-kit+ CD45+ population was determined to be of mast cell identity, while the C-kit+ CD45- population expressed mRNA of the endothelial lineage. Since the number of cells obtainable from biopsies was limited, a comparison between directly isolated and monolayer and explant cultured cells, respectively, was carried out. While both cultures retained a small population of mast cells, only monolayer culture produced a stable and relatively high percentage of C-kit+ CD45- cells. This population was found to co-express endothelial progenitor cell markers such as CD31, CD34, CXCR4, and FLK-1. The mRNA expression profile was similar to the one from directly isolated cells. When sorted cells were cultured in endothelial differentiation medium, the C-kit+ CD45- population retained its expression of endothelial markers to a large extent, but downregulated progenitor markers, indicating further differentiation into endothelial cells. We have confirmed that the human cardiac atrium contains a small C-kit+ CD45- population expressing markers commonly found on endothelial progenitor cells. The existence of an endothelial progenitor population within the heart might have future implications for developing methods of inducing neovascularization after myocardial infarction.
Basic Res Cardiol 2010 Jul
PMID:C-kit+ CD45- cells found in the adult human heart represent a population of endothelial progenitor cells. 2011 35

Metal-induced allergic reactions are not rare in every day practice but nickel, cobalt and chromium are the most common offenders. Other metal anions and metal alloys represent also emerging causes for hypersensitivity reaction in humans. The metal struts of endovascular and intracardiac devices are usually alloys containing nickel and constitute causes for allergic reactions with possible intracardiac and intracoronary mast cell activation resulting in the Kounis hypersensitivity coronary syndrome. Newer intracoronary stents avoid nickel thus making them less allergenic. It is advisable that, before any device implantation, careful history of any metal allergy should be taken and efforts should be made for the development of new devices with better biocompatibility.
Int J Cardiol 2010 Nov 19
PMID:Nickel allergy, Kounis syndrome and intracardiac metal devices. 1803 12


<< Previous 1 2 3 4 5 Next >>