Molecular sensors and modulators of thermoreception

Zhang, Xuming

doi:10.1080/19336950.2015.1025186

Cited by 40 publications

(33 citation statements)

References 123 publications

(158 reference statements)

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“…It seems unlikely that OxPAPC activates only the TRPV1 channels. Other channels are also required for heat sensation, for example, TRPM3, calcium activated chloride channel anoctamin 1 (Zhang, ) or TRPM2 (Tan and McNaughton, ). Except for activation of TRPA1 and TRPV1 channels by OxPAPC (Oehler et al ., ), OxPL species or 4‐HNE have not been studied activating these receptors.…”

Section: Discussionmentioning

confidence: 99%

Antinociception by the anti‐oxidized phospholipid antibody E06

Mohammadi

Oehler

Kloka

et al. 2018

British J Pharmacology

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These authors contributed equally. BACKGROUND AND PURPOSEROS and their downstream molecules such as oxidized phospholipids (OxPL) and 4-hydroxynonenal activate TRPA1 and TRPV1 (vanilloid 1) cation channels in vivo and in vitro shaping thermal and mechanical hypersensitivity in inflammatory pain. E06/T15 is a monoclonal autoantibody against oxidized phosphatidylcholine (OxPC) used in diagnostics in arteriosclerosis. Recently, we provided evidence that E06 also ameliorates inflammatory pain. Here, we studied E06 for local treatment against hypersensitivity evoked by endogenous and exogenous agonists of TRPA1 or TRPV1 channels. EXPERIMENTAL APPROACHWe utilized a combination of reflexive and complex behavioural pain measurements, live-cell calcium imaging and OxPC-binding assays. The lipid peroxidation metabolite 4-hydroxynonenal, hydrogen peroxide as a source of ROS, allyl isothiocyanate and capsaicin were used to activate their respective receptors. KEY RESULTSAll irritants induced thermal and mechanical hypersensitivity, spontaneous nocifensive and affective-motivational behaviour, as well as calcium influx in HEK TRPA1 -or HEK TRPV1 -cells and dorsal root ganglion neurons. E06 prevented prolonged mechanical hypersensitivity induced by all irritants except for H 2 O 2 . E06 did not alter immediate irritant-induced nocifensive or affective motivational behaviour. In vitro, E06 blocked only 4-hydroxynonenal-induced calcium influx although this compound did not bind to E06. After 1-3 h, all tested irritants elicited formation of OxPC in paw tissue. CONCLUSIONS AND IMPLICATIONSE06 ameliorates not only inflammatory pain but also prolonged hypersensitivity due to formation of OxPC. This supports the view that neutralizing certain OxPL as endogenous activators of TRPA1 or TRPV1 channels may be valuable for pain therapy. Abbreviations

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Section: Discussionmentioning

confidence: 99%

Antinociception by the anti‐oxidized phospholipid antibody E06

Mohammadi

Oehler

Kloka

et al. 2018

British J Pharmacology

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“…Thus, apart from TRPV1, a possible role of TRPV4 channel on human vascular regulation during exposure to warm environment cannot be excluded. Conversely, any effect of warm environment and capsaicin administration on blood pressure was not apparent in temperate condition, in which the activation of cold‐sensitive channels (TRPM8) may counteract vasorelaxation.…”

Section: Discussionmentioning

confidence: 99%

Effects of capsaicin application on the skin during resting exposure to temperate and warm conditions

Botonis

Miliotis

Kounalakis

et al. 2018

Scandinavian Med Sci Sports

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We investigated thermoregulatory and cardiovascular responses at rest in a temperate (20°C) and in a warm (30°C) environment (40% RH) without and with the application of capsaicin on the skin. We hypothesized that regardless of environmental temperature, capsaicin application would stimulate heat loss and concomitantly deactivate heat conservation mechanisms, thus resulting in rectal temperature (Tre) and mean blood pressure decline due to excitation of heat‐sensitive TRPV1. Ten male subjects were exposed, while seated, for 30 minutes to 20.8 ± 1.0°C or to 30.6 ± 1.1°C: without (NCA) and with (CA) application of capsaicin patches on the skin. Thermoregulatory (Tre, proximal‐distal skin temperature gradient) and cardiovascular variables (modelflow technique) as well as oxygen uptake were continuously measured. The area under the curve for Tre decline at 20°C was smaller in CA (−2.1 ± 1.3 a.u.) than in NCA (−0.6 ± 1.1 a.u., P < 0.01, r = 0.8). Likewise, at 30°C it was smaller in CA (−2.2 ± 2.1 a.u.) compared to NCA (−0.8 ± 2.0 a.u., P = 0.02, r = 0.7). Local vasomotor tone and oxygen uptake, were significantly lower by 36.7% ± 94.2% and 12.3% ± 12.3%, respectively, with capsaicin compared to NCA (P = 0.05 and P < 0.01, respectively). Additionally, in 30°C CA mean arterial pressure was lower by 10.7% ± 5.9%, 8.9% ± 5.9%, and 10.6% ± 7.0% compared to 30°C NCA, 20°C NCA, and 20°C CA, respectively (P < 0.01, P = 0.02, and P < 0.01, respectively, d = 1.4‐1.8). In conclusion, capsaicin application on the skin induced vasodilation and Tre decline. At 30°C CA, thermal responses were accompanied by arterial hypotension most likely due to the interactive effects of both stressors (warm environment and capsaicin) on cutaneous vascular regulation.

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“…They also respond to endogenous agents and messengers produced during tissue injury and inflammation [ 2 ]. TRP channels therefore function as molecular sensors responsible for detecting the external world and internal milieu, and have been implicated in diverse physiological processes and diseases, such as temperature sensation, vision, taste, pain, itch and cardiovascular diseases [ 1 , 2 , 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

“…The TRPV subfamily consists of six members. Of them, TRPV1–4 are mainly expressed in the sensory ganglia and skin responsible for thermo-sensation, pain and itch, whilst TRPV5 and TRPV6 are primarily expressed in the kidney and gastrointestinal tract and play a major role in Ca 2+ absorption and homeostasis [ 3 , 5 , 6 ]. The TRPM subfamily is the largest, consisting of eight members broadly expressed in a variety of cells and tissues, such as sensory ganglia, pancreatic beta cells, immune cells, the tongue, heart and kidney, and are critical for sensory physiology (e.g., heat (TRPM3), cold (TRPM8), taste (TRPM5) and light (TRPM1) sensing and detection) [ 5 ], insulin release (TRPM2, TRPM4 and TRPM5) [ 7 , 8 ], Mg 2+ homeostasis (TRPM6 and TRPM7), ischemic injury and inflammatory responses (TRPM2, TRPM4) [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Ca2+ Regulation of TRP Ion Channels

Hasan

Zhang

2018

IJMS

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Ca2+ signaling influences nearly every aspect of cellular life. Transient receptor potential (TRP) ion channels have emerged as cellular sensors for thermal, chemical and mechanical stimuli and are major contributors to Ca2+ signaling, playing an important role in diverse physiological and pathological processes. Notably, TRP ion channels are also one of the major downstream targets of Ca2+ signaling initiated either from TRP channels themselves or from various other sources, such as G-protein coupled receptors, giving rise to feedback regulation. TRP channels therefore function like integrators of Ca2+ signaling. A growing body of research has demonstrated different modes of Ca2+-dependent regulation of TRP ion channels and the underlying mechanisms. However, the precise actions of Ca2+ in the modulation of TRP ion channels remain elusive. Advances in Ca2+ regulation of TRP channels are critical to our understanding of the diversified functions of TRP channels and complex Ca2+ signaling.

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Molecular sensors and modulators of thermoreception

Cited by 40 publications

References 123 publications

Antinociception by the anti‐oxidized phospholipid antibody E06

Antinociception by the anti‐oxidized phospholipid antibody E06

Effects of capsaicin application on the skin during resting exposure to temperate and warm conditions

Ca2+ Regulation of TRP Ion Channels

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