Mast cells play a pivotal role in ischaemia reperfusion injury to skeletal muscles

Bortolotto, Susan K.; Morrison, Wayne A.; Han, Xiao-Lian; Messina, Aurora

doi:10.1038/labinvest.3700126

Cited by 36 publications

(39 citation statements)

References 27 publications

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“…Degranulating mast cells could potentially mediate this effect through yet-unknown mechanisms. CNS microvascular pathology has been described in ALS (69) and could lead to local hypoxia further promoting recruitment of mast cells, as has been reported in ischemia-reperfusion of skeletal muscle (70). A similar microcirculation failure has been reported in other neuromuscular pathologies such as spinal muscle atrophy or muscular dystrophy (71,72).…”

Section: Discussionmentioning

confidence: 76%

Evidence for mast cells contributing to neuromuscular pathology in an inherited model of ALS

Trías¹,

Ibarburu²,

Barreto-Núñez³

et al. 2017

JCI Insight

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Section: Discussionmentioning

confidence: 76%

Evidence for mast cells contributing to neuromuscular pathology in an inherited model of ALS

Trías¹,

Ibarburu²,

Barreto-Núñez³

et al. 2017

JCI Insight

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“…These data have led to the hypothesis that activation of the classical C pathway with formation of membrane-attack complexes leads to muscle injury. However, the finding that muscle damage is markedly attenuated in C-sufficient but mast cell (MC)-deficient B6D2F 1 (3)(4)(5) indicates that IR-mediated injury is a more complex pathologic response than currently understood and that MCs play a prominent role in this cytotoxic injury.…”

mentioning

confidence: 94%

“…Others have assessed muscle damage 24 h after reperfusion (3,5). To determine the time course of MC degranulation relative to skeletal muscle injury, we assessed each at 1, 3, and 6 h after the initiation of reperfusion in C57BL/6 mice.…”

Section: Time Course Of Muscle Injury and MC Degranulation After Repementioning

confidence: 99%

Mast Cell Protease 5 Mediates Ischemia-Reperfusion Injury of Mouse Skeletal Muscle

Abonia¹,

Friend²,

Austen

et al. 2005

The Journal of Immunology

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Ischemia with subsequent reperfusion (IR) injury is a significant clinical problem that occurs after physical and surgical trauma, myocardial infarction, and organ transplantation. IR injury of mouse skeletal muscle depends on the presence of both natural IgM and an intact C pathway. Disruption of the skeletal muscle architecture and permeability also requires mast cell (MC) participation, as revealed by the fact that IR injury is markedly reduced in c-kit defective, MC-deficient mouse strains. In this study, we sought to identify the pathobiologic MC products expressed in IR injury using transgenic mouse strains with normal MC development, except for the lack of a particular MC-derived mediator. Histologic analysis of skeletal muscle from BALB/c and C57BL/6 mice revealed a strong positive correlation (R2 = 0.85) between the extent of IR injury and the level of MC degranulation. Linkage between C activation and MC degranulation was demonstrated in mice lacking C4, in which only limited MC degranulation and muscle injury were apparent. No reduction in injury was observed in transgenic mice lacking leukotriene C4 synthase, hemopoietic PGD2 synthase, N-deacetylase/N-sulfotransferase-2 (enzyme involved in heparin biosynthesis), or mouse MC protease (mMCP) 1. In contrast, muscle injury was significantly attenuated in mMCP-5-null mice. The MCs that reside in skeletal muscle contain abundant amounts of mMCP-5 which is the serine protease that is most similar in sequence to human MC chymase. We now report a cytotoxic activity associated with a MC-specific protease and demonstrate that mMCP-5 is critical for irreversible IR injury of skeletal muscle.

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“…Bortolotto proved that ischemia-reperfusion injury was depending upon the presence of mast cells in skeletal muscle [2] .…”

Section: Introductionmentioning

confidence: 99%

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

Hei¹

2007

WJG

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AIM:To investigate the effects of Cromolyn Sodium (CS) pretreated prior to reperfusion on the activity of intestinal mucosal mast cells (IMMC) and mucous membrane of the small intestine in ischemia-reperfusion (IR) injury of rats. METHODS:Thirty-two Sprague-Dawley (SD) rats were randomly divided into four groups: sham group (group S), model group (group M), high and low dosage of CS groups, (treated with CS 50 mg/kg or 25 mg/kg, group C1 and C2). Intestinal IR damage was induced by clamping the superior mesenteric artery for 45 min followed by reperfusion for 60 min. CS was intravenouly administrated 15 min before reperfusion. Ultrastructure and counts of IMMC, intestinal structure, the expression of tryptase, levels of malondisldehyde (MDA), TNF-α, histamine and superoxide dismutase (SOD) activity of the small intestine were detected at the end of experiment. RESULTS:The degranulation of IMMC was seen in group M and was attenuated by CS treatment. Chiu's score of group M was higher than the other groups. CS could attenuate the up-regulation of the Chiu's score, the levels of MDA, TNF-α, and expression of tryptase and the down-regulation of SOD activity and histamine concentration. The Chiu's score and MDA content were negatively correlated, while SOD activity was positively correlated to the histamine concentration respectively in the IR groups. CONCLUSION:Pretreated of CS prior to reperfusion protects the small intestine mucous from ischemiareperfusion damage, the mechanism is inhibited IMMC from degranulation.

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Mast cells play a pivotal role in ischaemia reperfusion injury to skeletal muscles

Cited by 36 publications

References 27 publications

Evidence for mast cells contributing to neuromuscular pathology in an inherited model of ALS

Evidence for mast cells contributing to neuromuscular pathology in an inherited model of ALS

Mast Cell Protease 5 Mediates Ischemia-Reperfusion Injury of Mouse Skeletal Muscle

Pretreatment of cromolyn sodium prior to reperfusion attenuates early reperfusion injury after the small intestine ischemia in rats

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