Expression of Acid‐sensing Ion Channels of Gastric Mucosa From Patients With Henoch‐Schönlein Purpura

Yuan, Liping; Yan, Bo; Ming, Gui; Zhou, Qi-lian

doi:10.1097/mpg.0b013e318244255f

Cited by 6 publications

(2 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The ASIC subunits present in the gastrointestinal tract occur primarily on the peripheral fibres of extrinsic primary afferent neurons originating from the DRGs and nodose ganglia. There is only sparse information as to whether ASICs are also expressed by other cells such as oesophageal and gastric epithelial cells (Akiba et al, 2008; Yuan et al, 2012). Comparative functional and neurochemical studies indicate that ASIC-mediated currents in native sensory neurons are carried by ASIC1a and ASIC3 homomultimers (Escoubas et al, 2000; Sutherland et al, 2001), ASIC1b-containing channels (Diochot et al, 2012) as well as ASIC2a/ASIC3 and ASIC2b/ASIC3 heteromultimers (Waldmann et al, 1999; Xie et al, 2002; Diochot et al, 2004; Yagi et al, 2006).…”

Section: Expression Of Acid-sensing Ion Channels In the Gastrointementioning

confidence: 99%

“…This inference is consistent with the finding that the expression of ASIC3, but not ASIC1 and ASIC2, is enhanced in the colonic mucosa of patients with inflamed Crohn’s disease (Yiangou et al, 2001). Likewise, the immunocytochemical density of ASIC2 and ASIC3, but not ASIC1a, is increased in the gastric mucosa of patients with Henoch-Schönlein purpura, a vasculitis of immunological aetiology (Yuan et al, 2012). These clinical observations are matched by experimental findings that ASIC1a in rat DRG neurons and both ASIC1 and ASIC2 in the rat spinal cord are upregulated along with butyrate-induced hypersensitivity to colorectal distension (Matricon et al, 2011, 2013).…”

Section: Physiological and Pathophysiological Implications Of Acidmentioning

confidence: 99%

See 1 more Smart Citation

Acid-sensing ion channels in gastrointestinal function

Holzer

2015

Neuropharmacology

View full text Add to dashboard Cite

Gastric acid is of paramount importance for digestion and protection from pathogens but, at the same time, is a threat to the integrity of the mucosa in the upper gastrointestinal tract and may give rise to pain if inflammation or ulceration ensues. Luminal acidity in the colon is determined by lactate production and microbial transformation of carbohydrates to short chain fatty acids as well as formation of ammonia. The pH in the oesophagus, stomach and intestine is surveyed by a network of acid sensors among which acid-sensing ion channels (ASICs) and acid-sensitive members of transient receptor potential ion channels take a special place. In the gut, ASICs (ASIC1, ASIC2, ASIC3) are primarily expressed by the peripheral axons of vagal and spinal afferent neurons and are responsible for distinct proton-gated currents in these neurons. ASICs survey moderate decreases in extracellular pH and through these properties contribute to a protective blood flow increase in the face of mucosal acid challenge. Importantly, experimental studies provide increasing evidence that ASICs contribute to gastric acid hypersensitivity and pain under conditions of gastritis and peptic ulceration but also participate in colonic hypersensitivity to mechanical stimuli (distension) under conditions of irritation that are not necessarily associated with overt inflammation. These functional implications and their upregulation by inflammatory and non-inflammatory pathologies make ASICs potential targets to manage visceral hypersensitivity and pain associated with functional gastrointestinal disorders. This article is part of the Special Issue entitled 'Acid-Sensing Ion Channels in the Nervous System'.

show abstract

Section: Expression Of Acid-sensing Ion Channels In the Gastrointementioning

confidence: 99%

Section: Physiological and Pathophysiological Implications Of Acidmentioning

confidence: 99%

Acid-sensing ion channels in gastrointestinal function

Holzer

2015

Neuropharmacology

View full text Add to dashboard Cite

show abstract

Platelet-Rich Plasma and the Elimination of Neuropathic Pain

Kuffler

2013

Mol Neurobiol

View full text Add to dashboard Cite

Peripheral neuropathic pain typically results from trauma-induced nociceptive neuron hyperexcitability and their spontaneous ectopic activity. This pain persists until the trauma-induced cascade of events runs its full course, which results in complete tissue repair, including the nociceptive neurons recovering their normal biophysical properties, ceasing to be hyperexcitable, and stopping having spontaneous electrical activity. However, if a wound undergoes no, insufficient, or too much inflammation, or if a wound becomes stuck in an inflammatory state, chronic neuropathic pain persists. Although various drugs and techniques provide temporary relief from chronic neuropathic pain, many have serious side effects, are not effective, none promotes the completion of the wound healing process, and none provides permanent pain relief. This paper examines the hypothesis that chronic neuropathic pain can be permanently eliminated by applying platelet-rich plasma to the site at which the pain originates, thereby triggering the complete cascade of events involved in normal wound repair. Many published papers claim that the clinical application of platelet-rich plasma to painful sites, such as muscle injuries and joints, or to the ends of nerves evoking chronic neuropathic pain, a process often referred to as prolotherapy, eliminates pain initiated at such sites. However, there is no published explanation of a possible mechanism/s by which platelet-rich plasma may accomplish this effect. This paper discusses the normal physiological cascade of trauma-induced events that lead to chronic neuropathic pain and its eventual elimination, techniques being studied to reduce or eliminate neuropathic pain, and how the application of platelet-rich plasma may lead to the permanent elimination of neuropathic pain. It concludes that platelet-rich plasma eliminates neuropathic pain primarily by platelet- and stem cell-released factors initiating the complex cascade of wound healing events, starting with the induction of enhanced inflammation and its complete resolution, followed by all the subsequent steps of tissue remodeling, wound repair and axon regeneration that result in the elimination of neuropathic pain, and also by some of these same factors acting directly on neurons to promote axon regeneration thereby eliminating neuropathic pain.

show abstract