Role of stem cell factor and mast cells in the progression of chronic glomerulonephritides11See Editorial by Eddy, p. 375

El‐Koraie, Ahmed F.; Baddour, Nahed; Adam, Ahmed; Kashef, Essam H. El; Nahas, A. Meguid El

doi:10.1046/j.1523-1755.2001.00783.x

Cited by 50 publications

(43 citation statements)

References 25 publications

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“…In the study by El-Koraie et al, 22 mast cells and their associated growth factor (SCF) and receptor (c-kit) were present within the interstitium of scarred human kidneys and played a role in the initiation and progression of renal interstitial fibrosis. Frangogiannis et al 23 reported an increase in the number of mast cells in areas of collagen deposition and proliferating cell nuclear antigen expression and concluded that mast cells played an important role in myocardial remodeling and fibrosis after myocardial ischemia.…”

Section: Discussionmentioning

confidence: 99%

Mast Cells Play a Critical Role in the Pathogenesis of Viral Myocarditis

et al. 2008

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Section: Discussionmentioning

confidence: 99%

Mast Cells Play a Critical Role in the Pathogenesis of Viral Myocarditis

et al. 2008

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“…32 Evidence for a role of SCF in human airway disease was supported by studies demonstrating increased SCF expression in nasal polyps of asthmatics and allergic rhinitis patients. 33,34 Additionally, SCF has been implicated as a potential mediator in fibrotic diseases in the kidney and intestine. 34 -37 Recently, the role of SCF has been verified using a chronic Figure 4.…”

Section: Discussionmentioning

confidence: 99%

Eosinophil Activation of Fibroblasts from Chronic Allergen-Induced Disease Utilizes Stem Cell Factor for Phenotypic Changes

Dolgachev

Berlin

Lukacs

2008

The American Journal of Pathology

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In the present studies the role of stem cell factor (SCF) in mediating eosinophil and fibroblast activation during their interaction was investigated. SCF was significantly higher in fibroblasts grown from lungs of chronic allergen-challenged mice compared to fibroblasts grown from normal mice. When eosinophils were layered onto fibroblasts from allergic mice, a significant increase in SCF was detected compared to fibroblasts from nonallergic mice. The interaction of fibroblasts with eosinophils also increased the production of asthmaassociated chemokines, CCL5 and CCL6, was dependent on cell-to-cell interaction, and was observed only with fibroblasts derived from lungs of chronic allergen-challenged mice and not from those derived from unchallenged normal mice. Chemokine production was significantly decreased when anti-SCF antibodies were added during eosinophil-fibroblast interaction. The interaction of fibroblasts from chronic allergen-challenged mice with eosinophils also increased ␣-smooth muscle cell actin and procollagen I expression as well as induced transforming growth factor-␤. The changes in myofibroblast activation were dependent on SCF-mediated pathways because anti-SCF antibody treatment reduced the expression of all three of these latter fibrosisassociated markers. Thus , our data suggest that SCF mediates an important activation pathway for fibroblasts during chronic allergic responses on interaction with recruited eosinophils and suggest a potential mechanism of airway remodeling during chronic disease. Allergic airway inflammation is characterized by peribronchial eosinophil accumulation accompanied by mucus production and airway changes. Structural changes in the asthmatic airway include an increase in smooth muscle mass and deposition of extracellular matrix proteins. These changes correlate with airway hyperresponsiveness, reduced lung function, and an increase in fibroblast and myofibroblast numbers. These debilitating effects are not specifically targeted by current therapeutic agents, presenting a clinical challenge that might be better addressed by an enhanced understanding of the mechanisms. 1 In addition to contributing to airway remodeling, lung fibroblasts may also play a role in local regulation of immune and inflammatory responses. Fibroblasts are a potential source of granulocyte monocyte-colony stimulating factor (GM-CSF) and stem cell factor (SCF), known to promote differentiation, activation, and survival of eosinophils and mast cells. 2 Eosinophils have been shown to highly express c-kit (SCF receptor) on their surface. 3,4 We have previously shown that SCF is an important eosinophil-activating factor 4 that influences eosinophil recruitment in allergic airway inflammation. 5 SCF-induced activation of eosinophils has been shown to up-regulate expression of fibroblast growth factors, such as FGF5 and FGF7 (KGF). 4 Eosinophils also express at least two potent mediators [interleukin (IL)-1␤ and transforming growth factor (TGF)-␤] that induce a myofibroblast phenotype. The emergi...

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“…Mast cells, a rare cell population in healthy kidneys, increase in chronic inflammation and fibrosis, including that of allografts in which their numbers correlate with renal injury (48)(49)(50)(51). Most studies have suggested that a reduction of mast cells, or their typical enzyme chymase, increases fibrosis (52)(53)(54)(55)(56), whereas others suggest the opposite (57,58).…”

Section: The Role Of Immune Cellsmentioning

confidence: 99%