TRP-channel-specific cutaneous eicosanoid release patterns

  title={TRP-channel-specific cutaneous eicosanoid release patterns},
  author={Anila B. Jain and Simone Br{\"o}nneke and Ludger Kolbe and Franz Stäb and Horst Wenck and Gitta Neufang},

TRPV1 and TRPA1 in cutaneous neurogenic and chronic inflammation: pro-inflammatory response induced by their activation and their sensitization

The role of TRPV1 and TRPA1 in the modulation of inflammatory genes that leads to or maintains CNI in sensory neurons and non-neuronal skin cells is discussed.

Emerging roles of keratinocytes in nociceptive transduction and regulation

Keratinocytes serve as both sources and targets of neurotrophic factors, pro-inflammatory cytokines, and neuropeptides and create a bidirectional feedback loop that amplifies neuro inflammation and contributes to peripheral sensitization.

Epidermal expression of human TRPM8, but not of TRPA1 ion channels, is associated with sensory responses to local skin cooling.

The present observations demonstrating a lack of association of TRPA1 channel expression with cold sensitivity related measures reinforce doubts about involvement of this channel in cold pain in humans.

The TRPA1 channel in inflammatory and neuropathic pain and migraine.

Specific attention is paid to TRPA1 as the main contributing mechanism to the transition of mechanical and cold hypersensitivity from an acute to a chronic condition and as the primary transducing pathway by which oxidative/nitrative stress produces acute nociception, allodynia, and hyperalgesia.

Transient Receptor Potential Ankyrin 1 (TRPA1)—An Inflammation-Induced Factor in Human HaCaT Keratinocytes

Findings point to an inflammatory role for TRPA1 in keratinocytes and present TRPA 1 as a potential drug target in inflammatory skin diseases.

Transient receptor potential ankyrin 1 (TRPA1) is functionally expressed in primary human osteoarthritic chondrocytes

It is shown for the first time that TRPA1 is expressed in primary human OA chondrocytes and its expression is increased following stimulation with inflammatory factors IL-1β, IL-17, LPS, and resistin.

TRPA1 Sensitization Produces Hyperalgesia to Heat but not to Cold Stimuli in Human Volunteers

The observation that the TRPA1 irritant cinnamaldehyde induced heat hyperalgesia at an effect sizes comparable with that of capsaicin attributes TRPA 1 a role in human heat-induced pain suggests the inclusion of heat pain as a major efficacy measure in human experimental studies of the effects ofTRPA1 antagonists and the development of TRPA2 antagonists for clinical pain settings involving heat hyperAlgesia.

TRP channels in the skin

This review focuses on introducing the roles of several cutaneous TRP channels in the regulation of the skin barrier, skin cell proliferation and differentiation, and immune functions and describes the putative involvement of several TRPannels in the development of certain skin diseases.

TRP channels in skin: from physiological implications to clinical significances

Not only act in sensory processing, TRP channels also contribute to epidermal differentiation, proliferation, barrier integration, skin regeneration, and immune responses and might be good therapeutic targets in diseases with aberrantTRP channels.



Overexpressed Transient Receptor Potential Vanilloid 3 Ion Channels in Skin Keratinocytes Modulate Pain Sensitivity via Prostaglandin E2

A previously undescribed mechanism for keratinocytes participation in thermal pain transduction through keratinocyte TRPV3 ion channels and the intercellular messenger PGE2 is revealed.

Cox-dependent fatty acid metabolites cause pain through activation of the irritant receptor TRPA1

It is shown that cyclopentenone PGs produce pain by direct stimulation of nociceptors via TRPA1 activation, expanding the mechanism of NSAID analgesia from blockade of indirect nocceptor sensitization by classical PGs to inhibition of direct TRPA 1-dependent nocICEptor activation by cyclopENTenonePGs.

The Capsaicin Receptor TRPV1 Is a Crucial Mediator of the Noxious Effects of Mustard Oil

Prostaglandin-Induced Activation of Nociceptive Neurons via Direct Interaction with Transient Receptor Potential A1 (TRPA1)

Consistent with the hypothesis that TRPA1 activation required reactive electrophilic moieties, A- and J-series prostaglandins, and the isoprostane 8-iso-prostaglandin A2-evoked calcium influx in hTRPA1-HEK cells with similar potency and efficacy, data suggest a novel mechanism through which reactive prostanoids may activate nociceptive neurons independent of prostaglandsin receptors.

Mustard oils and cannabinoids excite sensory nerve fibres through the TRP channel ANKTM1

It is shown that mustard oil depolarizes a subpopulation of primary sensory neurons that are also activated by capsaicin, the pungent ingredient in chilli peppers, and by Δ9-tetrahydrocannabinol, the psychoactive component of marijuana.

Eicosanoid and cytokine levels in acute skin irritation in response to tape stripping and capsaicin.

A correlation was observed between levels of prostaglandin E2 and interleukin-1alpha in capsaicin pre-treated blister fluids (r=0.58, p<0.01, n=19).

Eicosanoid and cytokine levels in acute skin irritation in response to tape stripping and capsaicin.

A correlation was observed between levels of prostaglandin E2 and interleukin-1alpha in capsaicin pre-treated blister fluids (r=0.58, p<0.01, n=19).