TGFβ1 induces mast cell apoptosis

Norozian, Farnaz; Kashyap, Mohit; Ramı́rez, C.; Patel, Neha U.; Kepley, Christopher L.; Barnstein, Brian; Ryan, John

doi:10.1016/j.exphem.2006.02.003

Cited by 32 publications

(29 citation statements)

References 41 publications

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“…Treatment with TGFB1 elevates KIT mRNA levels in T-leukaemia cells and in melanoblasts (Tomeczkowski et al 1998, Kawakami et al 2002. In contrast to these two studies that reported a stimulatory impact, the capacity of TGFB1 to reduce KIT levels has been demonstrated in several systems (Heinrich et al 1995, Sansilvestri et al 1995, Hassan & Zander 1996, Bellone et al 1997, Norozian et al 2006). This repressive effect of TGFB1 on KIT may occur through accelerated degradation of KIT mRNA, rather than through a direct impact on mRNA synthesis (Dubois et al 1994, Heinrich et al 1995.…”

Section: Transforming Growth Factor B Superfamilymentioning

confidence: 58%

Control of KIT signalling in male germ cells: what can we learn from other systems?

Mithraprabhu¹,

Loveland²

2009

Reproduction

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The KIT ligand (KITL)/KIT-signalling system is among several pathways known to be essential for fertility. In the postnatal testis, the KIT/KITL interaction is crucial for spermatogonial proliferation, differentiation, survival and subsequent entry into meiosis. Hence, identification of endogenous factors that regulate KIT synthesis is important for understanding the triggers driving germ cell maturation. Although limited information is available regarding local factors in the testicular microenvironment that modulate KIT synthesis at the onset of spermatogenesis, knowledge from other systems could be used as a basis for identifying how KIT function is regulated in germ cells. This review describes the known regulators of KIT, including transcription factors implicated in KIT promoter regulation. In addition, specific downstream outcomes in biological processes that KIT orchestrates are addressed. These are discussed in relationship to current knowledge of mammalian germ cell development.

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Section: Transforming Growth Factor B Superfamilymentioning

confidence: 58%

Control of KIT signalling in male germ cells: what can we learn from other systems?

Mithraprabhu¹,

Loveland²

2009

Reproduction

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“…Recently, it was reported that TGF-1 is a potent apoptotic inducer of mast cells derived from mouse bone marrow cells, peritoneal cells and human skin cells. The cell death seen appears to be caused by TGF-mediated repression of IL-3 receptor expression, thus leading to mitochondrial damage and activation of an apoptotic cascade acting via p53 and caspases [113]. Under the conditions tested in our experiments, TGF-did antagonize the activities of IL-3 and SCF on mast cell growth and development.…”

Section: Other Cytokines Regulating Mast Cell De-velopmentmentioning

confidence: 87%

Regulation of Mast Cell Development by Inflammatory Factors

Zhao²,

Shimamura

2007

CMC

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Mast cells are potent effectors playing a key role in IgE-associated hypersensitivity reactions, allergic disorders, inflammation and protective immune responses. Mast cell development in vivo occurs mainly in non-hematopoietic microenvironments and increased mast cell numbers can be seen in various inflammatory diseases and pathologic conditions. SCF (also known as kit ligand or KitL) and c-kit signaling are essential for both human and murine mast cell development, while IL-3 is required for murine mast cell hyperplasia that occurs in response to various stimuli. Besides SCF and IL-3, the cytokines IL-4, IL-9, IL-10 and IL-13 are also called mast cell growth factors due to their actions synergistically promoting mast cell proliferation and differentiation in the presence of SCF or IL-3. These cytokines alone however are unable to support neither the proliferation nor survival of mast cells. Most research has focused on examining the direct effects of the above cytokines on mast cells or their precursors. However, it is difficult to explain the process of mast cell development only in terms of the above mast cell growth factors. A series of experiments in our laboratory and by others has revealed that inflammatory mediators and cytokines, as triggers or regulators, are also crucial for mast cell development. This review summarizes recent progress in our understanding of how various inflammatory factors regulate mast cell development, with particular focus on the effects of prostaglandin E (PGE), TNF-alpha, IL-6, IFN-gamma and an unknown apoptosis-inducing factor produced by IL-4-stimulated macrophages.

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“…148,149 On the other hand, TGF-␤ has been found to inhibit late-stage mast cell maturation 150,151 and induce mast cell apoptosis. 152 The bipolar effects of TGF-␤ on mast cells depend on the developmental stage at which mast cells are exposed to TGF-␤ and on the TGF-␤ concentration. 150,151 4.…”

Section: Tgf-␤mentioning

confidence: 99%

Immune Cells and Molecular Mediators in the Pathogenesis of the Abdominal Aortic Aneurysm

Rizas

Ippagunta²,

Tilson³

2009

Cardiology in Review

135

105

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Abdominal aortic aneurysm is a multifactorial disease with genetic risk factors and an immunologic component. Immune cells, including macrophages, neutrophils, mast cells, B- and T- lymphocytes, along with vascular smooth muscle cells and adventitial fibroblasts, produce cytokines and enzymes, promoting an inflammatory reaction, extracellular matrix degradation, and neovascularization. Among the different enzymes secreted by immune and stromal cells, matrix metalloproteinase (MMP)-2, MMP-9, MMP-12, cathepsins, and neutrophil elastase cause medial degeneration. Chymase causes smooth muscle cell apoptosis, and MMP-3, MMP-8, and MMP-13 cause adventitial collagen degradation, promoting abdominal aortic aneurysm rupture. At the same time chemokines (interleukin 8, macrophage inflammatory protein 1 alpha, monocyte chemotactic protein-1) cause recruitment and proliferation of inflammatory cells, whereas cytokines (vascular endothelial growth factor and transforming growth factor-beta) promote neoangiogenesis.

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TGFβ1 induces mast cell apoptosis

Cited by 32 publications

References 41 publications

Control of KIT signalling in male germ cells: what can we learn from other systems?

Control of KIT signalling in male germ cells: what can we learn from other systems?

Regulation of Mast Cell Development by Inflammatory Factors

Immune Cells and Molecular Mediators in the Pathogenesis of the Abdominal Aortic Aneurysm

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