Cloning and pharmacological characterization of mouse TRPV1

Correll, Craig C.; Phelps, P. Tara; Anthes, John C.; Umland, Shelby P.; Greenfeder, Scott

doi:10.1016/j.neulet.2004.07.058

Cited by 91 publications

(69 citation statements)

References 24 publications

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“…Phorbol 12-phenylacetate 13-acetate 20-homovanillate (PPAHV), a TRPV1 agonist, can stimulate rodent (19 -22) but not human TRPV1 (20). Capsazepine, a TRPV1 antagonist, does not antagonize proton-and heat-induced responses in rodent (20,21) but does antagonize in human (20) and porcine TRPV1 (16). Therefore, using a porcine orthologue may be more advantageous to predict physiological and pharmacological characteristics in human TRPV1.…”

mentioning

confidence: 99%

Novel Gating and Sensitizing Mechanism of Capsaicin Receptor (TRPV1)

Ohta

Imagawa

2008

Journal of Biological Chemistry

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Transient receptor potential V1 (TRPV1) is a nonselective cation channel expressed in nociceptors andsurrounding several proton-sensitive sites on the extracellular side of the pore-forming loop of the TRPV1 channel may play an important role as a brake to suppress the excessive activity of this channel under physiological conditions. Transient receptor potential V1 (TRPV1) 2 is a nonselective cation channel with high Ca 2ϩ permeability found in sensory neurons that functions as a molecular integrator of pain perception (1). TRPV1 is activated by polymodal stimuli such as capsaicin, protons, and noxious heat (2). Some endogenous ligands termed endovanilloids (3), including 15-hydroperoxyeicosa-5Z,8Z,11Z,13E-tetraenoic acid (15(S)-HPETE), a lipoxygenase product, also activate TRPV1 (4). Because mice genetically lacking the TRPV1 channel exhibit impaired nociception (5, 6) and several TRPV1 antagonists have antinociceptive activity in vivo (7-9), TRPV1 is considered to be a key component of signal transduction pathways in the nociceptive system. Several regulatory mechanisms of TRPV1 function have been elucidated. Sensitization can arise from phosphorylation of TRPV1 at multiple sites via protein kinase C and protein kinase A downstream of activation of GTP-binding protein-coupling receptor by bradykinin, ATP, nerve growth factor, calcitonin gene-related peptide, and prostaglandins (10). Our recent report also showed that the metabotropic 5-HT receptor facilitates TRPV1 functions through protein kinase C/protein kinase A pathways (11). TRPV1 is subject to tonic inhibition by phosphatidylinositol 4,5-bisphosphate (PIP 2 ) (12), providing an additional biochemical pathway through which the activity of the channel can be regulated after GTPbinding protein-coupling receptor activation. Recently, increases of cationic strength have been shown to contribute to inflammatory pain signaling through modulation of TRPV1 channels, since extracellular cations such as Na ϩ , Mg 2ϩ , and Ca 2ϩ gate and sensitize them (13). Hyponatremia, a disease due to reduction of the plasma Na ϩ concentration, is one of the most common electrolyte disorders (14). It occurs via excess loss of plasma Na ϩ as a result of various causes such as chronic renal failure and congestive heart failure. When the serum Na ϩ level falls gradually over a period of several days or weeks, sodium levels as low as 110 meq/liter may be reached with minimal symptomatology. Its symptoms are often concomitant with pain (15). However, the molecular detector of pain perception in hyponatremia has not yet been identified.We recently cloned a porcine orthologue of TRPV1 (pTRPV1) and analyzed its functional properties using a heterologous expression system (16). We showed that pTRPV1 was a nonselective cation channel sensitive to a number of vanilloid agonists, including capsaicin and endovanilloids, heat, and protons. In pharmacological characteristics of TRPV1, there are remarkable species differences; chicken TRPV1 is not sensitive * This work was supported by grants...

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confidence: 99%

Novel Gating and Sensitizing Mechanism of Capsaicin Receptor (TRPV1)

Ohta

Imagawa

2008

Journal of Biological Chemistry

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“…Others suggested that PMA-induced activation of PKC could only minimally activate TRPV1 (Crandall et al, 2002;Vellani et al, 2001) compared to capsaicinevoked activation. The study of Correll et al (2004) was in contrast with the previous one and found that PMA induced activation of TRPV1 is highly efficacious at the physiological temperature of 37°C and they were able to monitored and assessed the full induction of TRPV1 by a PKC-mediated pathway.…”

Section: Micementioning

confidence: 91%

“…The murine model was also used in the recent past to study the modulation of TRPV1 activation via Phorbol 12-Myristate 13-Acetate (PMA) inducing Protein Kinase C (PKC) phosphorylation. Some studies suggested that PMA can induce phosphorylation of PKC modulating TRPV1 activation and leading to a decrease of the heat threshold of TRPV1 activation from 42°C to 32°C that means that TRPV1 could also be activated at physiological temperatures and PKC-mediated phosphorylation should be sufficient to activate TRPV1 (Correll et al, 2004). Others suggested that PMA-induced activation of PKC could only minimally activate TRPV1 (Crandall et al, 2002;Vellani et al, 2001) compared to capsaicinevoked activation.…”

Section: Micementioning

confidence: 99%

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Transient Receptor Potential Vanilloid 1 Involvement in Animal Pain Perception

Vercelli¹,

Barbero²

2015

American Journal of Animal and Veterinary Sciences

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In last decades, Transient Receptor Potential Vanilloid 1 (TRPV1) has been the target of a large number of scientific investigations. It has been identified as a polymodal transducer molecule on a sub-set of primary sensory neurons which responds to various endogenous and exogenous stimuli including noxious heat (more than 42°C), protons and vanilloids such as capsaicin, the hot ingredient of chilli peppers. In mammals, TRPV1 displays a wide tissue and cellular expression including both the peripheral and central nervous system, with broad distribution and functions, in physiological and pathological conditions. Its primary localisation in sensory neurons reveals its key nodal point in pain transmission pathways. Nowadays, it is clear that TRPV1 is involved in inflammation, pain perception and thermoregulation in the majority of animals, including humans. Recently, a lot of studies tried to investigate some analgesic treatments applied on TRPV1. The aim of this review is to give to the readers a short overview of the TRPV1 involvement in pain perception and possible therapeutic applications, highlighting this topic in species of interest in veterinary medicine.

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“…Caterina and co-workers cloned TRPV1 from a rat sensory neuron cDNA library and showed that the receptor is expressed in both the dorsal root (DRG) and trigeminal ganglia (TG) [24]. TRPV1 has also been cloned from humans [25], guinea pigs [26], rabbits [27], mouse mice [28] and dogs [29].…”

Section: Trpvs: a Brief Overviewmentioning

confidence: 99%

Is TRPV1 a useful target in respiratory diseases?

Takemura

Quarcoo

Niimi

et al. 2008

Pulmonary Pharmacology & Therapeutics

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This review focuses on the transient receptor potential vanilloid 1 (TRPV1). TRPV1 is a non-selective cation channel predominantly expressed in the cell membranes of sensory afferent fibers, which are activated multi-modally. In the mammalian respiratory system, immunohistochemical and electrophysiological studies have revealed heterogeneous localizations of TRPV1 channels in the airways and their presence in pleural afferents. TRPV1 channels in afferents are not only involved with sensory inputs, but also release several neuropeptides upon stimulation. These processes trigger pathophysiological effects (e.g. reflex bronchoconstriction, hypersecretion, cough, etc.) that cause various symptoms of airway diseases.Recent studies have identified several endogenous and exogenous substances that can activate TRPV1 in the lung. Because of its key role in initiating inflammatory processes, TRPV1 receptor antagonists have been proposed as therapeutic candidates. Therefore, a critical update of recent therapeutic results is also given in this review.

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Cloning and pharmacological characterization of mouse TRPV1

Cited by 91 publications

References 24 publications

Novel Gating and Sensitizing Mechanism of Capsaicin Receptor (TRPV1)

Novel Gating and Sensitizing Mechanism of Capsaicin Receptor (TRPV1)

Transient Receptor Potential Vanilloid 1 Involvement in Animal Pain Perception

Is TRPV1 a useful target in respiratory diseases?

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