Mast cell/fibroblast interactions

Levi‐Schaffer, Francesca; Rubinchik, Evelina

doi:10.1111/j.1365-2222.1994.tb02737.x

Cited by 30 publications

(13 citation statements)

References 47 publications

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“…Adhesion of murine mast cell to fibroblast is well studied in vitro and seems to involve ckit and its ligand, the stem factor that has been implicated in mast cell proliferation and differentiation (Adachi et al 1992(Adachi et al , 1995Tsai et al 1991). Besides, there are strong arguments favoring reciprocal influences between mast cells and fibroblasts (Davidson et al 1983;Takeda et al 1989;Levi-Schaffer and Rubinchik 1994). Our data showing concentration of pinocytic vesicles in the fibroblast membrane in close apposition to mast cells suggest a functional interaction between these two opossum cells, as evidenced in the human lung (Heard et al 1992).…”

Section: Discussionmentioning

confidence: 95%

Mast cell types and cell-to-cell interactions in lymph nodes of the opossum Didelphis albiventris

Chiarini-Garcia¹,

Santos

Machado³

2000

Anatomy and Embryology

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Previous light-microscopic studies have shown a unique population of mast cells in lymphatic sinuses of lymph nodes located in the head, neck, axillary fossa and inguinal region of the opossum. In the present work, scanning and transmission electron-microscopic studies in the opossum mandibular and superficial axillary lymph nodes have strengthened the differences between connective-tissue mast cells (CTMC) and the lymphatic-sinus mast cells (LSMC). Further, close appositions of mast cells to other cells were described. At the nodal capsule, CTMC contacted fibroblast and granulocytes. In the lymphatic sinuses a few CTMC contacted LSMC, macrophages and reticular cells. The LSMC contacted macrophages, reticular cells and other LSMC. A few LSMC could be located in the medullary cord in close contact with plasma cells or other lymphoid cells, keeping the same ultrastructural features of those found in the lymphatic sinuses. An important new finding was provided by light-microscopic studies in nine abdominal lymph nodes. Most of them (para-aortic, common iliac, cardial, cecocolic and those of the body and tail of the pancreas) displayed numerous LSMC with the same distribution and histological features described herein. However, the mesenteric, pyloric and head-of-pancreas lymph nodes were virtually devoid of LSMC. Instead, their mast cells occurred mainly at the medullary cords and were very similar to the CTMC. Ultrastructural studies at the mesenteric lymph nodes confirmed the CTMC character of the mast cells located at both medullary cords and sinuses, and disclosed interactions with macrophages and lymphoid cells.

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Section: Discussionmentioning

confidence: 95%

Mast cell types and cell-to-cell interactions in lymph nodes of the opossum Didelphis albiventris

Chiarini-Garcia¹,

Santos

Machado³

2000

Anatomy and Embryology

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“…It has been previously shown that both ¢broblasts and smooth muscle cells, and/or products of these cell types, can also exert an e¡ect on mast cells, regulating their phenotype [Levi-Scha¡er and Rubinchik, 1994;LeviScha¡er and Weg, 1997;Mori et al, 1997;Welle, 1997]. Mast cell recruitment has been shown in response to transforming growth factor-b (TGF-b) and stem cell factor, cytokines which can be synthesized and secreted by both of these cell types.…”

Section: Discussionmentioning

confidence: 98%

Mast cell chymase is a possible mediator of neurogenic bladder fibrosis

Howard

Renfrow

Schechter³

et al. 2004

Neurourology and Urodynamics

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“…Both associative studies and experiments using mast cell deficient rodent models suggest an important role for mast cells in tissue fibrosis and extracellular matrix remodeling [73, 74]. The normal myocardium is populated by chymase and tryptase-positive mast cells that exhibit a distinct immunologic and biochemical phenotype [75].…”

Section: The Cellular Effectors Of Cardiac Fibrosismentioning

confidence: 99%

The pathogenesis of cardiac fibrosis

Kong

Christia

Frangogiannis

2013

Cell. Mol. Life Sci.

1,325

1,147

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Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review manuscript discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.

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Mast cell/fibroblast interactions

Cited by 30 publications

References 47 publications

Mast cell types and cell-to-cell interactions in lymph nodes of the opossum Didelphis albiventris

Mast cell types and cell-to-cell interactions in lymph nodes of the opossum Didelphis albiventris

Mast cell chymase is a possible mediator of neurogenic bladder fibrosis

The pathogenesis of cardiac fibrosis

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