Are mast cells involved in hypertensive heart disease?

Panizo, Ángel; Mindan, F. J. Pardo; Galindo, Marı́a F.; Cenarruzabeitia, Edurne; Hernández, Marta; Dı́ez, Javier

doi:10.1097/00004872-199510000-00015

Cited by 68 publications

(52 citation statements)

References 18 publications

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“…For example, chymase may elicit antifibrinogenic actions by activating pro-MMP-1 (31), and tryptase can activate pro-MMP-3, which initiates activation of multiple MMPs (12). In contrast, other mast cell-derived mediators such as cytokines promote fibroblast proliferation and collagen production (15,26).…”

Section: Discussionmentioning

confidence: 99%

“…Mast cells may also play a role in hypertensive heart disease. Although changes in mast cell number were not observed in hearts from a Goldblatt model of hypertension in rats (30), studies in spontaneously hypertensive rats led investigators to suggest that mast cells play a role in the cardiac fibrosis and hypertrophy that occur in hypertension, possibly due to the secretion of cytokines and growth factors (26,32). Experiments also showed that the progression from compensated hypertrophy to decompensated failure in a pressure overload model is largely prevented in mast celldeficient mice or in wild-type mice treated with tranilast, a mast cell stabilizer (15).…”

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confidence: 99%

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Cardiac function in hearts isolated from a rat model deficient in mast cells

Kennedy

Hauer‐Jensen²,

Joseph³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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2004.-Several studies have examined the role of mast cells in the myocardial response to injury such as that caused by hypertension and ischemia-reperfusion. However, little is known about the influence of mast cells on normal myocardial structure and function. The present experiments examined cardiac function in Langendorff-perfused hearts isolated from 6-and 9-mo-old male mast cell-deficient (Ws/Ws) and mast cell-competent rats. A fluid-filled balloon catheter was used to measure left ventricular diastolic and systolic function at increasing preload volumes. At 6 mo of age, mast cell-deficient rats showed a slight cardiac hypertrophy (as monitored by heart weight and heart weight-to-body weight ratio) but no significant change in maximum observed systolic or diastolic function. In contrast, at 9 mo of age, the mast cell-deficient group showed no signs of hypertrophy but displayed a diastolic dysfunction characterized by decreased compliance without a significant decline in maximum observed basal ϪdP/dt max. There were no significant differences in maximum observed values for measures of systolic function (developed pressure and ϩdP/dtmax). In summary, the results of this study in adult rats suggest that mast cells influence cardiac function in the absence of injury and that observed differences between mast cell-competent and -deficient animals vary with age. Thus it is important to consider these "physiological" actions and resulting changes in function when studying effects of insult in mast cell-deficient models.compliance; diastolic dysfunction; Langendorff-perfused hearts MAST CELLS are part of the innate immune system that provides the first line of defense against tissue damage. In addition to their critical role in immunoglobulin E-dependent, histaminemediated hypersensitivity, mast cells release and modulate cytokines, growth factors, chemokines, proteases, and other mediators, which in turn regulate a vast array of important biological processes. Many mast cell mediators (e.g., histamine, heparin, tryptase, chymase, TNF-␣, and interleukin-4) are preformed and stored in large amounts in secretory granules, available for immediate release (21). Studies have demonstrated that mast cells reside in the myocardium even under physiological conditions, with their distribution along the coronary capillaries being more dense in the arteriolar section (30).Several studies have examined the potential role of mast cells in the myocardial response to injury. However, in many cases, the results of these studies have been contradictory. For example, numerous investigators have monitored the contribution of mast cells to preconditioning as well as ischemic injury. Parikh and Singh (27, 28) suggested that ischemia-and norepinephrine-induced preconditioning are mediated in part by degranulation of resident mast cells in the rat heart, whereas Wang et al. (37) reported that mast cell degranulation is not involved in ischemic cardiac preconditioning in rabbits. Similarly, the role of mast cells in the acute tissue damage...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cardiac function in hearts isolated from a rat model deficient in mast cells

Kennedy

Hauer‐Jensen²,

Joseph³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…These cells have also been demonstrated to be associated with various cardiovascular inflammatory conditions, including hypertensive cardiac hypertrophy [14], ischemia-reperfusion injury [15], ischemic cardiomyopathy [16] and cardiac allograft rejection [17]. In 1968, Fernex [18] [DOI 10.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of mast cells by interleukin‐10 gene transfer contributes to protection against acute myocarditis in rats

Palaniyandi

Watanabe

et al. 2004

Eur J Immunol

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Progression of acute myocarditis involves a variety of inflammatory events. Mast cells have been implicated as the source of various cytokines, chemokines and histamine in acute inflammation and fibrosis. Interleukin (IL)-10 has well-known immunomodulatory actions that are exerted during the recovery phase of myocarditis. In this study, 9-week-old male Lewis rats were immunized with cardiac myosin. A plasmid vector expressing mouse IL-10 cDNA (800 lg per rat) was then transferred three times (7, 12 and 17 days after immunization) into the tibialis anterior muscles of the rats by electroporation. Microscopic examination of mast cells was carried out on toluidine blue-stained transverse sections of the mid ventricles. Mouse IL-10 gene transfer significantly reduced mast cell density, cardiac histamine concentration and mast cell growth, and prevented mast cell degranulation. Furthermore, improvement in both myocardial function and the overall condition of the rats was evident from the reduction in the heart weight-to-body weight ratio and inflammatory infiltration as well as improvement in hemodynamic and echocardiographic parameters. These findings suggest that IL-10 gene transfer by electroporation protected against myocarditis via mast cell inhibition.

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“…The fibrogenic role of mast cells in idiopathic pulmonary fibrosis, 1) neurofibroma 2) and cutaneous fibrosis 3) has been demonstrated. Recently, mast cells have been implicated in myocardial fibrosis of hypertensive hypertrophy, 4) ischemia-reperfusion 5) and postcardiac transplantation. 6) Progressive interstitial fibrosis is an essential component of left ventricular remodeling in patients with chronic heart failure.…”

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confidence: 99%