Rat cardiac mast cell maturation and differentiation following acute ventricular volume overload

Forman, Mary F.; Brower, Gregory L.; Janicki, Joseph S.

doi:10.1007/s00011-006-6016-z

Cited by 21 publications

(21 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, by using the pericardial sac as a structure analogous to the peritoneal cavity, we have developed a protocol that consistently produces a high yield of functional epicardial mast cells. Importantly, as can be seen in Figure 4, the mast cells thus obtained are phenotypically consistent with the tryptase and chymase positive MC TC subset of connective tissue mast cells previously described in myocardial tissue [20,22,24,28,29].…”

Section: Discussionsupporting

confidence: 56%

A novel technique for isolating functional mast cells from the heart

et al. 2008

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 56%

A novel technique for isolating functional mast cells from the heart

et al. 2008

Self Cite

View full text Add to dashboard Cite

show abstract

“…Based on this observation, they hypothesized that chemotaxis of circulating mast cell precursors may have been responsible for the mast cell accumulation. An alternative possibility is suggested by recent observations from our laboratory demonstrating the rapid maturation of resident cardiac mast cell precursors [54]. The maturation and differentiation of resident mast cell precursors are known to be associated with progressive sulfation of heparin and the formation of mast cell chymase and histamine.…”

Section: Role Of Cardiac Mast Cells In the Activation Of Mmpsmentioning

confidence: 95%

“…Using this technique, a significant decrease in immature or stages I and II and a significant increase in mature or stages III and IV cardiac mast cells relative to sham-operated rats were observed within 24 h of initiating a volume overload. Furthermore, this shift from immature to mature mast cell did not occur in AV fistula rats that were treated with a mast cell stabilizing drug [54].…”

Section: Role Of Cardiac Mast Cells In the Activation Of Mmpsmentioning

confidence: 98%

Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload

Janicki

Brower

Gardner

et al. 2006

Cardiovascular Research

100

View full text Add to dashboard Cite

The chronic elevation in ventricular wall stress secondary to ventricular volume or pressure overload leads to structural remodeling of the muscular, vascular and extracellular matrix components of the myocardium. While initially a compensatory response, the progressive hypertrophy and ventricular dilatation induced by this condition ultimately have a detrimental effect on ventricular function, resulting in heart failure. Fibrillar collagen provides the skeletal framework which interconnects the cardiomyocytes, thereby maintaining ventricular shape and size and contributing to tissue stiffness. Accordingly, these myocardial collagen fibers must be disrupted for ventricular dilatation, sphericalization and wall thinning to occur. The presence of an abundant, latent matrix metalloproteinase (MMP) population which coexists with myocardial fibrillar collagen has been documented. Thus, the potential for collagen degradation to exceed synthesis exists should there be significant activation of this latent MMP system. Mast cells are known to store and release a variety of biologically active mediators including TNF-alpha and proteases such as tryptase and chymase, which can induce MMP activation. Increased cardiac mast cell density has been implicated in the pathophysiology of human end-stage cardiomyopathy and experimental myocardial infarction, hypertension and chronic volume overload secondary to mitral regurgitation and aorto-caval fistula. The potential role of cardiac mast cells in activating MMPs, which then results in fibrillar collagen degradation and adverse myocardial remodeling secondary to chronic volume and pressure overload will be the subject of this review.

show abstract

“…However, another potential source of this increased mast cell density is the rapid maturation of immature, resident mast cells. We recently found chronic volume overload induced maturation/differentiation of cardiac mast cells in rats with an AV fistula (14). Four stages (I-IV) of mast cell maturation have been identified using differential staining of mast cells.…”

Section: Mast Cell Density Postfistulamentioning

confidence: 99%

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

Murray

Gardner²,

Brower³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Murray DB, Gardner JD, Brower GL, Janicki JS. Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cellmediated ventricular remodeling in rats. Am J Physiol Heart Circ Physiol 294: H1251-H1257, 2008. First published January 4, 2008 doi:10.1152/ajpheart.00622.2007.-The objective of this study was to investigate the effect a nonselective endothelin-1 (ET-1) receptor antagonist (bosentan) had on the acute myocardial remodeling process including left ventricular (LV) mast cells and matrix metalloproteinase (MMP) activity secondary to volume overload. Additionally, we investigated the overall functional outcome of preventative endothelin receptor antagonism during 14 days of chronic volume overload. LV tissue from sham-operated (Sham), untreated-fistula (Fist), and bosentan (100 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 )-treated animals (Fist ϩ Bos) was analyzed for mast cell density, MMP activity, and myocardial collagen volume fraction at 1 and 5 days after the creation of an aortocaval fistula. When compared with untreated fistulas, bosentan treatment prevented the marked increase in LV mast cell density at 1 day postfistula (3.1 Ϯ 0.3 vs. 1.3 Ϯ 0.3 LV mast cells/mm 2 , Fist vs. Fist ϩ Bos, P Յ 0.01). Additionally, the substantial increase in MMP-2 activation in the untreated fistula at 1 day was prevented following bosentan treatment (1.6 Ϯ 0.3 vs. 0.9 Ϯ 0.1 arbitrary activity units, Fist vs. Fist ϩ Bos, P Յ 0.01). The marked decrease in collagen volume fraction seen in the Fist group (1.4 Ϯ 0.1 vs. 0.8 Ϯ 0.1% myocardial tissue, Sham vs. Fist, P Յ 0.01) was significantly attenuated following bosentan treatment at both the 1-and 5-day time points. Lastly, a 2-wk preventative treatment with bosentan resulted in significant attenuation of the increase in LV end-systolic and -diastolic volumes compared with those in untreated fistula hearts. In summary, nonselective ET-1 antagonism prevents the acute increases in cardiac mast cell density and MMP activation induced secondary to chronic volume overload. By preventing these events, ET-1 antagonism was efficacious in attenuating ventricular dilatation and limiting the development of structural and functional deficits in the first 2 wk of chronic volume overload. Accordingly, these results are the first to demonstrate that cardiac mast cells are responsive to the endogenous endothelin system in vivo. Another novel finding from this study is that chronic nonspecific endothelin antagonism may inadvertently potentiate ET-1-mediated signaling.bosentan; heart; extracellular matrix; cardiac function DISCOVERED ONLY 16 years ago, the neurohormone endothelin-1 (ET-1) has been intensely investigated due to its potent cardiovascular effects and strong association with the pathophysiological worsening of cardiac function in congestive heart failure (7,13,16,29,35). ET-1 is a 21 amino acid peptide predominantly synthesized and secreted by endothelial cells. The effects of ET-1 are dictated by binding to one of two G protein-linked receptor subtypes A or B (ET A or ET B ) (16). In th...

show abstract

Rat cardiac mast cell maturation and differentiation following acute ventricular volume overload

Abstract: We conclude that the acute increase in mast cell density following volume overload is due to a paracrine response in the heart that stimulates the maturation and differentiation of resident immature cardiac mast cells.

Cited by 21 publications

References 28 publications

A novel technique for isolating functional mast cells from the heart

A novel technique for isolating functional mast cells from the heart

Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats

Contact Info

Product

Resources

About