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

To explore how cardiac regeneration and cell turnover adapts to disease, different forms of stress were studied for their effects on the cardiac progenitor cell markers c-Kit and Isl1, the early cardiomyocyte marker Nkx2.5, and mast cells. Adult female rats were examined during pregnancy, after myocardial infarction and ischemia-reperfusion injury with/out insulin like growth factor-1(IGF-1) and hepatocyte growth factor (HGF). Different cardiac sub-domains were analyzed at one and two weeks post-intervention, both at the mRNA and protein levels. While pregnancy and myocardial infarction up-regulated Nkx2.5 and c-Kit (adjusted for mast cell activation), ischemia-reperfusion injury induced the strongest up-regulation which occurred globally throughout the entire heart and not just around the site of injury. This response seems to be partly mediated by increased endogenous production of IGF-1 and HGF. Contrary to c-Kit, Isl1 was not up-regulated by pregnancy or myocardial infarction while ischemia-reperfusion injury induced not a global but a focal up-regulation in the outflow tract and also in the peri-ischemic region, correlating with the up-regulation of endogenous IGF-1. The addition of IGF-1 and HGF did boost the endogenous expression of IGF and HGF correlating to focal up-regulation of Isl1. c-Kit expression was not further influenced by the exogenous growth factors. This indicates that there is a spatial mismatch between on one hand c-Kit and Nkx2.5 expression and on the other hand Isl1 expression. In conclusion, ischemia-reperfusion injury was the strongest stimulus with both global and focal cardiomyocyte progenitor cell marker up-regulations, correlating to the endogenous up-regulation of the growth factors IGF-1 and HGF. Also pregnancy induced a general up-regulation of c-Kit and early Nkx2.5+ cardiomyocytes throughout the heart. Utilization of these pathways could provide new strategies for the treatment of cardiac disease.
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PMID:Ischemia-reperfusion injury and pregnancy initiate time-dependent and robust signs of up-regulation of cardiac progenitor cells. 2259 Jun 12

The concurrence of acute coronary syndrome with allergy or hypersensitivity as well as with anaphylactic or anaphylactoid reactions is increasingly encountered in daily clinical practice. There are several reports associating mast cell activation with acute cardiovascular events in adults. This was first described by Kounis as 'allergic angina syndrome',progressing to 'allergic myocardial infarction'. The main mechanism proposed is the vasospasm of coronary arteries. We present a case of a 28-year-old man who was admitted to our hospital with thoracic pain and dyspnoea. The symptoms recurred after simultaneous use of 1 g amoxicillin/clavulanic acid orally and 1 g ampicillin/sulbactam parenterally for tonsillitis the night before presentation and on the morning of admission.
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PMID:Kounis syndrome secondary to simultaneous oral amoxicillin and parenteral ampicillin use in a young man. 2315 96

The primary purpose of this review is to address the progress towards small molecule modulators of human Transient Receptor Potential Canonical proteins (TRPC1, TRPC3, TRPC4, TRPC5, TRPC6 and TRPC7). These proteins generate channels for calcium and sodium ion entry. They are relevant to many mammalian cell types including acinar gland cells, adipocytes, astrocytes, cardiac myocytes, cochlea hair cells, endothelial cells, epithelial cells, fibroblasts, hepatocytes, keratinocytes, leukocytes, mast cells, mesangial cells, neurones, osteoblasts, osteoclasts, platelets, podocytes, smooth muscle cells, skeletal muscle and tumour cells. There are broad-ranging positive roles of the channels in cell adhesion, migration, proliferation, survival and turning, vascular permeability, hypertrophy, wound-healing, hypo-adiponectinaemia, angiogenesis, neointimal hyperplasia, oedema, thrombosis, muscle endurance, lung hyper-responsiveness, glomerular filtration, gastrointestinal motility, pancreatitis, seizure, innate fear, motor coordination, saliva secretion, mast cell degranulation, cancer cell drug resistance, survival after myocardial infarction, efferocytosis, hypo-matrix metalloproteinase, vasoconstriction and vasodilatation. Known small molecule stimulators of the channels include hyperforin, genistein and rosiglitazone, but there is more progress with inhibitors, some of which have promising potency and selectivity. The inhibitors include 2-aminoethoxydiphenyl borate, 2-aminoquinolines, 2-aminothiazoles, fatty acids, isothiourea derivatives, naphthalene sulfonamides, N-phenylanthranilic acids, phenylethylimidazoles, piperazine/piperidine analogues, polyphenols, pyrazoles and steroids. A few of these agents are starting to be useful as tools for determining the physiological and pathophysiological functions of TRPC channels. We suggest that the pursuit of small molecule modulators for TRPC channels is important but that it requires substantial additional effort and investment before we can reap the rewards of highly potent and selective pharmacological modulators.
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PMID:In pursuit of small molecule chemistry for calcium-permeable non-selective TRPC channels -- mirage or pot of gold? 2376 62

"Kounis syndrome" refers to acute coronary syndromes of varying degree (myocardial ischaemia to infarction) induced by mast cell activation as a result of allergic and anaphylactic reactions. ST-segment elevated myocardial infarction is a rare complication that can occur even in patients with normal coronary arteries due to anaphylactic reactions. We present a case that developed acute myocardial infarction following a diclofenac sodium-induced anaphylaxis. The patient did not have any previous coronary artery disease, but there was a temporal relationship with development of the anaphylactic reaction due to diclofenac sodium and the cardiac event. The patient was managed conservatively and the recovery was uneventful.
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PMID:Kounis syndrome resulting from anaphylaxis to diclofenac. 2398 88

Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation following an allergic insult. We report a 56-year-old man who experienced a ST-segment elevation myocardial infarction after wasp stings. The patient presented without signs of anaphylaxis or shock. Coronary angiography showed an everolimus-eluting stent thrombosis (ST) of the left anterior descending artery occluding the vessel completely which was deployed for stable angina 3 years ago. The patient had been compliant with anti-platelet therapy, and no relevant cardiovascular events occurred until the day of admission. We interpreted our patient's condition as a manifestation of Kounis syndrome. To our knowledge, this is the first case of Kounis syndrome showing very late ST in a second-generation drug-eluting stent caused by wasp stings.
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PMID:Kounis syndrome presenting as very late stent thrombosis in an everolimus-eluting stent following wasp stings. 2404 16

Myocardial infarction as a result of wasp stings is a rare manifestation of acute coronary syndromes. It has been ascribed to kounis syndrome or allergic angina whose triggers include mast cell degranulation leading to coronary vasospasm and/or local plaque destabilisation. Its exact pathophysiology is still not clearly defined. We present a case of an acute coronary syndrome as a consequence of wasp stings and discuss its possible aetiology.
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PMID:Anaphylaxis from wasp stings inducing coronary thrombus. 2482 69

Rupture of an atherosclerotic plaque is the major underlying cause of adverse cardiovascular events such as myocardial infarction or stroke. Therapeutic interventions should therefore be directed towards inhibiting growth of atherosclerotic lesions as well as towards prevention of lesion destabilization. Interestingly, the presence of mast cells has been demonstrated in both murine and human plaques, and multiple interventional murine studies have pointed out a direct role for mast cells in early and late stages of atherosclerosis. Moreover, it has recently been described that activated lesional mast cells correlate with major cardiovascular events in patients suffering from cardiovascular disease. This review focuses on the effect of different mast cell derived mediators in atherogenesis and in late stage plaque destabilization. Also, possible ligands for mast cell activation in the context of atherosclerosis are discussed. Finally, we will elaborate on the predictive value of mast cells, together with therapeutic implications, in cardiovascular disease.
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PMID:The role of mast cells in atherosclerosis. 2537 48

Cardiac mast cells store and release a variety of biologically active mediators, several of which have been implicated in the activation of matrix metalloproteinases in the volume-overloaded heart, while others are involved in the fibrotic process in pressure-overloaded hearts. Increased numbers of mast cells have been reported in explanted human hearts with dilated cardiomyopathy and in animal models of experimentally induced hypertension, myocardial infarction, and chronic cardiac volume overload. Also, there is evolving evidence implicating the cardiac mast cell as having a major role in the adverse remodeling underlying these cardiovascular disorders. Thus, the cardiac mast cell is the focus of this chapter that begins with a historical background, followed by sections on methods for their isolation and characterization, endogenous secretagogues, phenotype, and ability of estrogen to alter their phenotype so as to provide cardioprotection. Finally the role of mast cells in myocardial remodeling secondary to a sustained cardiac volume overload, hypertension, and ischemic injury and future research directions are discussed.
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PMID:The emerging prominence of the cardiac mast cell as a potent mediator of adverse myocardial remodeling. 2538 48

Kounis syndrome is not a rare but an infrequently diagnosed non-thrombogenic cause of angina or myocardial infarction triggered by the release of inflammatory mediators following an allergic or anaphylactic reaction. This so-called "allergic angina" is seen in the setting of anaphylactic reactions and is believed to be due to mast cell release causing coronary vasospasm. The treatment of such cases is often with epinephrine, which has also been described in the literature as another rare cause of coronary vasospasm. We present a case of Kounis syndrome seen in a 46 year-old male who suffered two bee stings while landscaping in his yard. He developed an anaphylactic reaction and was promptly treated with IM epinephrine injection by paramedics at arrival and developed marked ST elevations on EKG in the inferior leads with reciprocal ST depressions in the anterior leads. His troponin peaked at 13 ng/mL and tryptase level was 15 ng/mL (normal <10 ng/mL). Coronary catheterisation showed non-diseased coronary arteries and a normal ejection fraction without evidence of vasospasm. He was afterwards treated with an epinephrine drip for distributive shock. Interestingly this syndrome was not provoked when re-challenged with this therapy, suggestive of an allergic reaction rather than epinephrine as the aetiology of his presumed vasospasm. This patient's ST segment elevation and troponin elevation was due to Kounis syndrome. Awareness that anaphylactic reactions can lead to Kounis syndrome can lead to prompt appropriate treatment for this life threatening condition.
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PMID:Kounis syndrome: a stinging case of ST-elevation myocardial infarction. 2554 29

Cardiovascular disease (CVD) increases the risk of severe or fatal anaphylaxis, and some medications for CVD treatment can exacerbate anaphylaxis. The aim of this article is to review the effect of anaphylaxis on the heart, the potential impact of medications for CVD on anaphylaxis and anaphylaxis treatment, and the cardiovascular effects of epinephrine. The therapeutic dilemmas arising from these issues are also discussed and management strategies proposed. PubMed searches were performed for the years 1990-2014 inclusive, using terms such as angiotensin-converting enzyme (ACE) inhibitors, adrenaline, allergic myocardial infarction, anaphylaxis, angiotensin-receptor blockers (ARBs), beta-adrenergic blockers, epinephrine, and Kounis syndrome. Literature analysis indicated that: cardiac mast cells are key constituents of atherosclerotic plaques; mast cell mediators play an important role in acute coronary syndrome (ACS); patients with CVD are at increased risk of developing severe or fatal anaphylaxis; and medications for CVD treatment, including beta-adrenergic blockers and ACE inhibitors, potentially exacerbate anaphylaxis or make it more difficult to treat. Epinephrine increases myocardial contractility, decreases the duration of systole relative to diastole, and enhances coronary blood flow. Its transient adverse effects include pallor, tremor, anxiety, and palpitations. Serious adverse effects (including ventricular arrhythmias and hypertension) are rare, and are significantly more likely after intravenous injection than after intramuscular injection. Epinephrine is life-saving in anaphylaxis; second-line medications (including antihistamines and glucocorticoids) are not. In CVD patients (especially those with ACS), the decision to administer epinephrine for anaphylaxis can be difficult, and its benefits and potential harms need to be carefully considered. Concerns about potential adverse effects need to be weighed against concerns about possible death from untreated anaphylaxis, but there is no absolute contraindication to epinephrine injection in anaphylaxis.
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PMID:Anaphylaxis and cardiovascular disease: therapeutic dilemmas. 2658 55


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