Cyclical mechanical stretch enhances degranulation and IL‐4 secretion in RBL‐2H3 mast cells

Komiyama, Hidenori; Miyake, Keisuke; Asai, Kuniya; Mizuno, Kyoichi; Shimada, Takashi

doi:10.1002/cbf.2973

Cited by 7 publications

(6 citation statements)

References 46 publications

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“…However, if these phenomena are excessive, or collagen fibers deposited in a random manner at the site of the lesion, local fibrosis could occur 17 . Our results are opposite to those found in other studies that caused mechanical tension in cells cultures 14,18 . This may have occurred due to the type of intervention, intensity and time of use of NM maneuvers.…”

Section: Discussioncontrasting

confidence: 57%

Neurodynamic Mobilization Reduces Intraneural Fibrosis After Sciatic Crush Lesion in Rats

Lima

Santana

Medrado

et al. 2017

BJMHH

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| Peripheral nerve lesions may be associated with abnormal scarring that lead to regenerative failure and dysfunction. Neurodynamic mobilization (NM) imposes controlled mechanical loads on the peripheral nerve and may influence inflammation and collagen deposition after a lesion. However, there is lack of experimental data to support these claims. Objective: To evaluate the impact of NM in the intraneural number of mast cells, collagen deposition and number of blood vessels after an ischiatic crush lesion in rats. Methods: This is a laboratory animal study, where 20 rats (Rattus norvegicus) were randomly divided into two groups, NM (n=10) and control (n=10), submitted to a right ischiatic nerve lesion. A tensioning NM began 10 days after lesion, and was maintained once a day, six times a week, for three weeks. After this period, the animals were euthanized and the nerves assessed for the number of mast cells, collagen area and number of blood vessels. Results: NM led to a lower number of degranulated mast cells (Kruskal-Wallis = 0.29 p<0.05), higher organization of collagen deposition (KruskalWallis = 0.01, p<0.05 ). There was no influence of NM on the number of intraneural blood vessels (KruskalWallis = 0.46 p<0.05). Conclusion: NM started 10 days after a ischiatic nerve crush lesion modulates the inflammatory process and prevents random deposition of collagen at the lesion site, but has no influence on blood vessels formation.

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Section: Discussioncontrasting

confidence: 57%

Neurodynamic Mobilization Reduces Intraneural Fibrosis After Sciatic Crush Lesion in Rats

Lima

Santana

Medrado

et al. 2017

BJMHH

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“…Rat mast cell line (RBL-2H3) was purchased from the cell bank of the Chinese Academy of Sciences (Shanghai, China) and was cultured in Eagle's minimum essential medium containing 10% fetal bovine serum, supplemented with 100 U/mL penicillin and 100 μ g/mL streptomycin at 37°C in a humidified atmosphere of 5% CO 2 as described [ 22 ]. A rat small intestinal epithelial cell line (IEC-6) was also obtained from the cell bank of the Chinese Academy of Sciences (Shanghai, China).…”

Section: Methodsmentioning

confidence: 99%

Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation

Gan

Xing

et al. 2015

Oxidative Medicine and Cellular Longevity

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Both oxidative stress and mast cell (MC) degranulation participate in the process of small intestinal ischemia reperfusion (IIR) injury, and oxidative stress induces MC degranulation. Propofol, an anesthetic with antioxidant property, can attenuate IIR injury. We postulated that propofol can protect against IIR injury by inhibiting oxidative stress subsequent from NADPH oxidase mediated MC activation. Cultured RBL-2H3 cells were pretreated with antioxidant N-acetylcysteine (NAC) or propofol and subjected to hydrogen peroxide (H2O2) stimulation without or with MC degranulator compound 48/80 (CP). H2O2 significantly increased cells degranulation, which was abolished by NAC or propofol. MC degranulation by CP further aggravated H2O2 induced cell degranulation of small intestinal epithelial cell, IEC-6 cells, stimulated by tryptase. Rats subjected to IIR showed significant increases in cellular injury and elevations of NADPH oxidase subunits p47phox and gp91phox protein expression, increases of the specific lipid peroxidation product 15-F2t-Isoprostane and interleukin-6, and reductions in superoxide dismutase activity with concomitant enhancements in tryptase and β-hexosaminidase. MC degranulation by CP further aggravated IIR injury. And all these changes were attenuated by NAC or propofol pretreatment, which also abrogated CP-mediated exacerbation of IIR injury. It is concluded that pretreatment of propofol confers protection against IIR injury by suppressing NADPH oxidase mediated MC activation.

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“…We assumed here the ATP and 5-HT co-release by meningeal immune cells (exemplified as mast cells). Mast cells react to mechanical stimuli (Zhang et al, 2012;Komiyama et al, 2014), which can serve as a signal to release the content of their secretory granules including ATP (Wang et al, 2013) to activate neighboring nerve fibers (Wang et al, 2015). Interestingly, cortical spreading depression (which underlies migraine aura, Charles, 2018), also degranulates mast cells and opens pannexin channels as the pathway for ATP release (Karatas et al, 2013).…”

Section: Potential Pathophysiological Implications In Migrainementioning

confidence: 99%

Modeling a Nociceptive Neuro-Immune Synapse Activated by ATP and 5-HT in Meninges: Novel Clues on Transduction of Chemical Signals Into Persistent or Rhythmic Neuronal Firing

Suleimanova

Talanov

Gafurov

et al. 2020

Front. Cell. Neurosci.

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Extracellular ATP and serotonin (5-HT) are powerful triggers of nociceptive firing in the meninges, a process supporting headache and whose cellular mechanisms are incompletely understood. The current study aimed to develop, with the neurosimulator NEURON, a novel approach to explore in silico the molecular determinants of the long-lasting, pulsatile nature of migraine attacks. The present model included ATP and 5-HT release, ATP diffusion and hydrolysis, 5-HT uptake, differential activation of ATP P2X or 5-HT3 receptors, and receptor subtype-specific desensitization. The model also tested the role of branched meningeal fibers with multiple release sites. Spike generation and propagation were simulated using variable contribution by potassium and sodium channels in a multi-compartment fiber environment. Multiple factors appeared important to ensure prolonged nociceptive firing potentially relevant to long-lasting pain. Crucial roles were observed in: (i) co-expression of ATP P2X2 and P2X3 receptor subunits; (ii) intrinsic activation/inactivation properties of sodium Nav1.8 channels; and (iii) temporal and spatial distribution of ATP/5-HT release sites along the branches of trigeminal nerve fibers. Based on these factors we could obtain either persistent activation of nociceptive firing or its periodic bursting mimicking the pulsating nature of pain. In summary, our model proposes a novel tool for the exploration of peripheral nociception to test the contribution of clinically relevant factors to headache including migraine pain.

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Cyclical mechanical stretch enhances degranulation and IL‐4 secretion in RBL‐2H3 mast cells

Cited by 7 publications

References 46 publications

Neurodynamic Mobilization Reduces Intraneural Fibrosis After Sciatic Crush Lesion in Rats

Neurodynamic Mobilization Reduces Intraneural Fibrosis After Sciatic Crush Lesion in Rats

Propofol Attenuates Small Intestinal Ischemia Reperfusion Injury through Inhibiting NADPH Oxidase Mediated Mast Cell Activation

Modeling a Nociceptive Neuro-Immune Synapse Activated by ATP and 5-HT in Meninges: Novel Clues on Transduction of Chemical Signals Into Persistent or Rhythmic Neuronal Firing

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