Role of Acid-Sensing Ion Channel 3 in Sub-Acute-Phase Inflammation

Yen, Yi-Tin; Tu, Pan-Hsien; Chen, Chien-Ju; Lin, Yi‐Wen; Hsieh, Sung‐Tsang; Chen, Chih‐Cheng

doi:10.1186/1744-8069-5-1

Cited by 105 publications

(95 citation statements)

References 38 publications

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“…Chen et al further noted an up regulation of ASIC3 channels in DRG neurons following carrageenan and CFA models of inflammation in mice, a phenomenon stopped and reversed by DN at ST36 [158]. At first glance, these findings suggest that DN may exploit the mechanical aspects of the receptor to reverse hyperalgesia.…”

Section: Asic Channelsmentioning

confidence: 97%

“…A number of studies have linked ASIC3 to mechanical but not heat hyperalgesia following carrageenan-induced inflammation and a series of acid injections [157,158]. Chen et al further noted an up regulation of ASIC3 channels in DRG neurons following carrageenan and CFA models of inflammation in mice, a phenomenon stopped and reversed by DN at ST36 [158].…”

Section: Asic Channelsmentioning

confidence: 99%

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Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Butts¹,

Dunning²

2016

Int J Phys Med Rehabil

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There are a number of biochemical, biomechanical, endocrinological and neurovascular mechanisms underpinning the anti-nociceptive and anti-inflammatory effects of dry needling (DN). While myofascial trigger points likely play a role in peripheral pain, a diagnostic tool for localizing them has not been validated, and DN studies that have targeted trigger points to elicit localized twitch responses have reported mixed results. Therefore, the mechanism responsible for DN-mediated analgesia may be more complicated. DN activates opioid-based pain reduction, mediated by endogenous cannabinoids and the sympathetic nervous system, and non-opioid pain relief via serotonin and norepinephrine from the brain stem. DN also triggers the hypothalamic-pituitary-adrenal axis centrally and the corticotropin releasing hormone-proopiomelanocortin-corticosteroid axis locally to inhibit cox-2, reducing inflammatory cytokines. Recent studies demonstrate that DN combined with mechanical and/or electrical stimulation may reverse PKC-mediated peripheral hyperalgesic priming by normalizing nociceptive channels, to include TRPV, ASIC, TTX and P2X/Y. Electrical DN (EDN) stimulates immune cells, fibroblasts and keratinocytes to release CGRP and substance-P, altering the stimulation of TTX receptors to reverse hyperalgesia. It also encourages the supraoptic nucleus to release oxytocin to quiet ASIC receptors peripherally and stimulate opioid interneurons spinally. Moreover, EDN inhibits ERK1/2 kinase pathways of inflammation in the spinal cord and stimulates Aδ fibers and N/OFQ to reverse C-fiber mediated central changes. Mechanotransduction of fibroblasts and peripheral nerves via TRPV1 and P2X/Y-mediated intracellular Ca 2+ wave propagation and subsequent activation of the nucleus accumbens inhibits spinal pain transmission via glycinergic and opioidergic interneurons. The increased ATP is metabolized to adenosine, which activates P1 purinergic receptors, events considered key to DN analgesia and rho kinase-based tissue remodeling. Mechanotransduction-mediated release of histamine further explains analgesia secondary to needling points distal to pain. DN-mediated analgesia is dependent on a number of synergistic physiologic events involving biochemical and mechanical processes in neural, connective and muscle tissue.

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Section: Asic Channelsmentioning

confidence: 97%

Section: Asic Channelsmentioning

confidence: 99%

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Butts¹,

Dunning²

2016

Int J Phys Med Rehabil

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“…Thus, peripheral ASIC3 channels are essential sensors of acidic pain and integrators of molecular signals produced during inflammation when they contribute to primary hyperalgesia in rats. More recently, Yen et al (55) reinvestigated the role of ASIC3 in primary hyperalgesia through more comprehensive behavioral analysis and pathological evaluation in mice. These authors concluded that ASIC3 participated in the maintenance of subacute-phase primary hyperalgesia in subcutaneous inflammation in mice (55).…”

Section: Cutaneous Nociceptionmentioning

confidence: 99%

“…More recently, Yen et al (55) reinvestigated the role of ASIC3 in primary hyperalgesia through more comprehensive behavioral analysis and pathological evaluation in mice. These authors concluded that ASIC3 participated in the maintenance of subacute-phase primary hyperalgesia in subcutaneous inflammation in mice (55). Compared with the wild-type (WT) mice, asic3 -/-mice showed normal thermal and mechanical hyperalgesia in acute (4-h) intraplantar complete Freund's adjuvant (CFA)-or carrageenan-induced inflammation, but the hyperalgesic effects in the subacute phase (1-2 days) were milder in all paradigms except for thermal hyperalgesia with CFA-induced inflammation.…”

Section: Cutaneous Nociceptionmentioning

confidence: 99%

ASIC3 Channels in Multimodal Sensory Perception

2010

ACS Chem. Neurosci.

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Acid-sensing ion channels (ASICs), which are members of the sodium-selective cation channels belonging to the epithelial sodium channel/degenerin (ENaC/ DEG) family, act as membrane-bound receptors for extracellular protons as well as nonproton ligands. At least five ASIC subunits have been identified in mammalian neurons, which form both homotrimeric and heterotrimeric channels. The highly proton sensitive ASIC3 channels are predominantly distributed in peripheral sensory neurons, correlating with their roles in multimodal sensory perception, including nociception, mechanosensation, and chemosensation. Different from other ASIC subunit composing ion channels, ASIC3 channels can mediate a sustained window current in response to mild extracellular acidosis (pH 7.3-6.7), which often occurs accompanied by many sensory stimuli. Furthermore, recent evidence indicates that the sustained component of ASIC3 currents can be enhanced by nonproton ligands including the endogenous metabolite agmatine. In this review, we first summarize the growing body of evidence for the involvement of ASIC3 channels in multimodal sensory perception and then discuss the potential mechanisms underlying ASIC3 activation and mediation of sensory perception, with a special emphasis on its role in nociception. We conclude that ASIC3 activation and modulation by diverse sensory stimuli represent a new avenue for understanding the role of ASIC3 channels in sensory perception. Furthermore, the emerging implications of ASIC3 channels in multiple sensory dysfunctions including nociception allow the development of new pharmacotherapy.

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“…Studies have shown that after injecting carrageenan into rat paws to induce tissue inflammation, neutrophils and macrophages gather at the inflammation site and induce cellular infiltration [25,31,32]. Neutrophils and macrophages mediate inflammatory responses in many diseases by expressing pro-inflammatory proteins that promote tissue inflammation [33].…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory and Analgesic Effects of the Marine-Derived Compound Comaparvin Isolated from the Crinoid Comanthus bennetti

et al. 2014

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To date, no study has been conducted to explore the bioactivity of the crinoid Comanthus bennetti. Here we report the anti-inflammatory properties of comaparvin (5,8-dihydroxy-10-methoxy-2-propylbenzo[h]chromen-4-one) based on in vivo experiments. Our preliminary screening for anti-inflammatory activity revealed that the crude extract of Comanthus bennetti significantly inhibited the expression of pro-inflammatory proteins in lipopolysaccharide (LPS)-stimulated murine RAW 264.7 macrophage cells. Comaparvin isolated from crinoids significantly decreased the expression of inducible nitric oxide synthase (iNOS) protein and mRNA in LPS-stimulated macrophage cells. Moreover, our results showed that post-treatment with comaparvin significantly inhibited mechanical allodynia, thermal hyperalgesia and weight-bearing deficits in rats with carrageenan-induced inflammation. Comaparvin also attenuated leukocyte infiltration and iNOS protein expression in carrageenan-induced inflamed paws. These results suggest that comaparvin is a potential anti-inflammatory therapeutic agent against inflammatory pain.

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Role of Acid-Sensing Ion Channel 3 in Sub-Acute-Phase Inflammation

Cited by 105 publications

References 38 publications

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

Peripheral and Spinal Mechanisms of Pain and Dry Needling Mediated Analgesia: A Clinical Resource Guide for Health Care Professionals

ASIC3 Channels in Multimodal Sensory Perception

Anti-Inflammatory and Analgesic Effects of the Marine-Derived Compound Comaparvin Isolated from the Crinoid Comanthus bennetti

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