Mast cell involvement in the progression of peritoneal fibrosis in rats with chronic renal failure

Kazama, Itsuro; Baba, Asuka; Endo, Yasuhiro; Toyama, Hiroaki; Ejima, Yutaka; Matsubara, Mitsunobu; Tachi, Masahiro

doi:10.1111/nep.12489

Cited by 20 publications

(36 citation statements)

References 29 publications

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“…The mast cell suspension was scattered in a chamber placed on the headstage of an inverted microscope (Nikon, Tokyo, Japan). As we carefully showed in our previous studies [13,14,18], single mast cells were easily distinguishable from other cells by their intracellular inclusion of secretory granules [13,14] or the positive staining for toluidine blue [18]. as described in our previous studies [13,14].…”

Section: Cell Sources and Preparationmentioning

confidence: 91%

“…Therefore, for the treatment or protection against such fibrosis, several pharmacological approaches to inhibit the activation of mast cells have been suggested, including the use of mast cell stabilizers [54,55] or chemokine inhibitors [56,57]. Recently, using rat models of chronic renal failure (CRF), we demonstrated that mast cells proliferated in situ within the fibrotic peritoneum and increased their production of fibroblast-activating factors [18]. Since treatment with tranilast actually ameliorated the progression of peritoneal fibrosis, mast cells were thought to be responsible for the progression of peritoneal fibrosis in CRF.…”

Section: Discussionmentioning

confidence: 99%

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Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Baba

Tachi²,

Ejima³

et al. 2016

Cell Physiol Biochem

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Background: Anti-allergic drugs, such as tranilast and ketotifen, inhibit the release of chemokines from mast cells. However, we know little about their direct effects on the exocytotic process of mast cells. Since exocytosis in mast cells can be monitored electrophysiologically by changes in the whole-cell membrane capacitance (Cm), the absence of such changes by these drugs indicates their mast cell-stabilizing properties. Methods: Employing the standard patch-clamp whole-cell recording technique in rat peritoneal mast cells, we examined the effects of tranilast and ketotifen on the Cm during exocytosis. Using confocal imaging of a water-soluble fluorescent dye, lucifer yellow, we also examined their effects on the deformation of the plasma membrane. Results: Relatively lower concentrations of tranilast (100, 250 µM) and ketotifen (1, 10 µM) did not significantly affect the GTP-γ-S-induced increase in the Cm. However, higher concentrations of tranilast (500 µM, 1 mM) and ketotifen (50, 100 µM) almost totally suppressed the increase in the Cm, and washed out the trapping of the dye on the surface of the mast cells. Compared to tranilast, ketotifen required much lower doses to similarly inhibit the degranulation of mast cells or the increase in the Cm. Conclusions: This study provides electrophysiological evidence for the first time that tranilast and ketotifen dose-dependently inhibit the process of exocytosis, and that ketotifen is more potent than tranilast in stabilizing mast cells. The mast cell-stabilizing properties of these drugs may be attributed to their ability to counteract the plasma membrane deformation in degranulating mast cells.

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Section: Cell Sources and Preparationmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Baba

Tachi²,

Ejima³

et al. 2016

Cell Physiol Biochem

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“…Eosinophils secrete profibrotic cytokines such as IL-13, IL-4, transforming growth factor (TGF)-, and stem cell factor which in turn induce fibroblast and mast cells proliferation and activation (215, 222, 223). Activated mast cells promote tissue remodeling and fibrosis by secreting tryptase, chymase, and histamine, which work closely with fibroblasts (Figure 5) (215, 224–226). As seen in the figure, monocytes and macrophages become activated and secrete several inflammatory and toxic mediators including MMPs (200, 227–232).…”

Section: The Proposed Mechanisms and Future Perspectives Of Soot- Andmentioning

confidence: 99%

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

2017

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The environmental soot and carbon blacks (CBs) cause many diseases in humans, but their underlying mechanisms of toxicity are still poorly understood. Both are formed after the incomplete combustion of hydrocarbons but differ in their constituents and percent carbon contents. For the first time, “Sir Percival Pott” described soot as a carcinogen, which was subsequently confirmed by many others. The existing data suggest three main types of diseases due to soot and CB exposures: cancer, respiratory diseases, and cardiovascular dysfunctions. Experimental models revealed the involvement of oxidative stress, DNA methylation, formation of DNA adducts, and Aryl hydrocarbon receptor activation as the key mechanisms of soot- and CB-induced cancers. Metals including Si, Fe, Mn, Ti, and Co in soot also contribute in the reactive oxygen species (ROS)-mediated DNA damage. Mechanistically, ROS-induced DNA damage is further enhanced by eosinophils and neutrophils via halide (Cl− and Br−) dependent DNA adducts formation. The activation of pulmonary dendritic cells, T helper type 2 cells, and mast cells is crucial mediators in the pathology of soot- or CB-induced respiratory disease. Polyunsaturated fatty acids (PUFAs) were also found to modulate T cells functions in respiratory diseases. Particularly, telomerase reverse transcriptase was found to play the critical role in soot- and CB-induced cardiovascular dysfunctions. In this review, we propose integrated mechanisms of soot- and CB-induced toxicity emphasizing the role of inflammatory mediators and oxidative stress. We also suggest use of antioxidants and PUFAs as protective strategies against soot- and CB-induced disorders.

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“…Rats with 5/6 nephrectomy and 8‐week recovery periods were used as the model of CRF in the present study. Subtotal nephrectomy was performed in male Sprague–Dawley rats weighing 150–180 g (Japan SLC Inc., Shizuoka, Japan) as described in our previous studies . Briefly, the upper third and lower third of the right kidney were ligated to induce infarction.…”

Section: Methodsmentioning

confidence: 99%

“…CKD is nowadays regarded as a disease of systemic inflammation and several studies recently demonstrated increased activity of peripheral mast cells in addition to T‐lymphocytes or macrophages . In our most recent study, mast cells were actually increased and activated in CRF rat peritoneum, and were thought to be responsible for the progression of peritoneal fibrosis . However, despite accumulating evidence that mast cells may infiltrate into the kidneys with chronic inflammation, we know little about their contribution to the pathogenesis of renal fibrosis associated with CRF.…”

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confidence: 90%

Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure

Baba

Tachi²,

Ejima

et al. 2017

Nephrology

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Mast cell involvement in the progression of peritoneal fibrosis in rats with chronic renal failure

Cited by 20 publications

References 29 publications

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways

Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure

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