Ion Channels and Thermosensitivity: TRP, TREK, or Both?

Lamas, José Antonio; Rueda‐Ruzafa, Lola; Herrera-Pérez, Salvador

doi:10.3390/ijms20102371

Cited by 69 publications

(57 citation statements)

References 101 publications

(275 reference statements)

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“…The TRP superfamily consists of the following six subfamilies, which are based on sequence homology: ankyrin-rich (TRPA1), vanilloid (TRPV1-6), canonical (TRPC1-7), melastatin-like (TRPM1-8), polycystin (TRPP2/3/5), and mucolipin (TRPML1-3) [57]. Their localization is ubiquitary, and they can be activated by a wide number of molecules and stimuli [56,58,59]. In endometrial biopsies, TRP expression levels have been reported to be differently down-and upregulated during the different phases of the menstrual cycle [60].…”

Section: Transient Receptor Potential (Trp) Channels and Endometriosismentioning

confidence: 99%

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Riemma

Laganà

Schiattarella

et al. 2020

IJMS

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Background: Ion channels play a crucial role in many physiological processes. Several subtypes are expressed in the endometrium. Endometriosis is strictly correlated to estrogens and it is evident that expression and functionality of different ion channels are estrogen-dependent, fluctuating between the menstrual phases. However, their relationship with endometriosis is still unclear. Objective: To summarize the available literature data about the role of ion channels in the etiopathogenesis of endometriosis. Methods: A search on PubMed and Medline databases was performed from inception to November 2019. Results: Cystic fibrosis transmembrane conductance regulator (CFTR), transient receptor potentials (TRPs), aquaporins (AQPs), and chloride channel (ClC)-3 expression and activity were analyzed. CFTR expression changed during the menstrual phases and was enhanced in endometriosis samples; its overexpression promoted endometrial cell proliferation, migration, and invasion throughout nuclear factor kappa-light-chain-enhancer of activated B cells-urokinase plasminogen activator receptor (NFκB-uPAR) signaling pathway. No connection between TRPs and the pathogenesis of endometriosis was found. AQP5 activity was estrogen-increased and, through phosphatidylinositol-3-kinase and protein kinase B (PI3K/AKT), helped in vivo implantation of ectopic endometrium. In vitro, AQP9 participated in extracellular signal-regulated kinases/p38 mitogen-activated protein kinase (ERK/p38 MAPK) pathway and helped migration and invasion stimulating matrix metalloproteinase (MMP)2 and MMP9. ClC-3 was also overexpressed in ectopic endometrium and upregulated MMP9. Conclusion: Available evidence suggests a pivotal role of CFTR, AQPs, and ClC-3 in endometriosis etiopathogenesis. However, data obtained are not sufficient to establish a direct role of ion channels in the etiology of the disease. Further studies are needed to clarify this relationship.

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Section: Transient Receptor Potential (Trp) Channels and Endometriosismentioning

confidence: 99%

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Riemma

Laganà

Schiattarella

et al. 2020

IJMS

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“…These studies have led to the identification of a number of ion channels activated by a wide spectrum of physical and chemical stimuli. Those activated by temperature belong to a superfamily of ion channels called transient receptor potential (TRP) channels [68,69]. Four TRP subtypes are activated by an increase in temperature and two TRP channels are activated by decreases in temperature [68].…”

Section: Neuronal Control Of Body Temperaturementioning

confidence: 99%

“…Those activated by temperature belong to a superfamily of ion channels called transient receptor potential (TRP) channels [68,69]. Four TRP subtypes are activated by an increase in temperature and two TRP channels are activated by decreases in temperature [68]. For example, TRPM8 is an ion channel that admits Ca2 + and Na + in response to moderate cold (10-25 • C), while several transient receptor potential cation channels (TRV) have been proposed to sense warmth including TRVP1, TRVP3, TRCP4 and TRVP2 [70].…”

Section: Neuronal Control Of Body Temperaturementioning

confidence: 99%

Impact of Adaptive Thermogenesis in Mice on the Treatment of Obesity

Bastías-Pérez

Zagmutt

Soler‐Vázquez

et al. 2020

Cells

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Obesity and associated metabolic diseases have become a priority area of study due to the exponential increase in their prevalence and the corresponding health and economic impact. In the last decade, brown adipose tissue has become an attractive target to treat obesity. However, environmental variables such as temperature and the dynamics of energy expenditure could influence brown adipose tissue activity. Currently, most metabolic studies are carried out at a room temperature of 21 °C, which is considered a thermoneutral zone for adult humans. However, in mice this chronic cold temperature triggers an increase in their adaptive thermogenesis. In this review, we aim to cover important aspects related to the adaptation of animals to room temperature, the influence of housing and temperature on the development of metabolic phenotypes in experimental mice and their translation to human physiology. Mice studies performed in chronic cold or thermoneutral conditions allow us to better understand underlying physiological mechanisms for successful, reproducible translation into humans in the fight against obesity and metabolic diseases.

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“…The study of TREK currents in native neurons is challenging because the activity of these channels is reduced at room temperature and atmospheric pressure [28][29][30]. We take advantage of the neuroprotective agent riluzole, which activates the three members of the TREK subfamily (TREK-1, TREK-2 and TRAAK (TWIK-related arachidonic acid-stimulated potassium channel)) [31][32][33][34].…”

Section: Introductionmentioning

confidence: 99%

PIP2 Mediated Inhibition of TREK Potassium Currents by Bradykinin in Mouse Sympathetic Neurons

Rivas-Ramírez

Reboreda

Rueda‐Ruzafa

et al. 2020

IJMS

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Bradykinin (BK), a hormone inducing pain and inflammation, is known to inhibit potassium M-currents (IM) and to increase the excitability of the superior cervical ganglion (SCG) neurons by activating the Ca2+-calmodulin pathway. M-current is also reduced by muscarinic agonists through the depletion of membrane phosphatidylinositol 4,5-biphosphate (PIP2). Similarly, the activation of muscarinic receptors inhibits the current through two-pore domain potassium channels (K2P) of the “Tandem of pore-domains in a Weakly Inward rectifying K+ channel (TWIK)-related channels” (TREK) subfamily by reducing PIP2 in mouse SCG neurons (mSCG). The aim of this work was to test and characterize the modulation of TREK channels by bradykinin. We used the perforated-patch technique to investigate riluzole (RIL) activated currents in voltage- and current-clamp experiments. RIL is a drug used in the palliative treatment of amyotrophic lateral sclerosis and, in addition to blocking voltage-dependent sodium channels, it also selectively activates the K2P channels of the TREK subfamily. A cell-attached patch-clamp was also used to investigate TREK-2 single channel currents. We report here that BK reduces spike frequency adaptation (SFA), inhibits the riluzole-activated current (IRIL), which flows mainly through TREK-2 channels, by about 45%, and reduces the open probability of identified single TREK-2 channels in cultured mSCG cells. The effect of BK on IRIL was precluded by the bradykinin receptor (B2R) antagonist HOE-140 (d-Arg-[Hyp3, Thi5, d-Tic7, Oic8]BK) but also by diC8PIP2 which prevents PIP2 depletion when phospholipase C (PLC) is activated. On the contrary, antagonizing inositol triphosphate receptors (IP3R) using 2-aminoethoxydiphenylborane (2-APB) or inhibiting protein kinase C (PKC) with bisindolylmaleimide did not affect the inhibition of IRIL by BK. In conclusion, bradykinin inhibits TREK-2 channels through the activation of B2Rs resulting in PIP2 depletion, much like we have demonstrated for muscarinic agonists. This mechanism implies that TREK channels must be relevant for the capture of information about pain and visceral inflammation.

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Ion Channels and Thermosensitivity: TRP, TREK, or Both?

Cited by 69 publications

References 101 publications

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Ion Channels in The Pathogenesis of Endometriosis: A Cutting-Edge Point of View

Impact of Adaptive Thermogenesis in Mice on the Treatment of Obesity

PIP2 Mediated Inhibition of TREK Potassium Currents by Bradykinin in Mouse Sympathetic Neurons

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