P2Y Receptor Linked to Phospholipase C: Stimulation of Neuro 2A Cells by UTP and ATP and Possible Regulation by Protein Kinase C Subtype ε

Chen, Ching-Chow; Chen, Wei-Chyuan

doi:10.1046/j.1471-4159.1997.69041409.x

Cited by 20 publications

(8 citation statements)

References 22 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results show that ATP mobilizes the intracellular Ca 2+ exclusively from ER pool activated via G q /G 11 -protein/PLC/IP 3 pathway. This is consistent with the earlier report by Chen and Chen (1997), which showed the inositol triphosphate formation in Neuro2a cells stimulated by P2Y receptor agonists.…”

Section: Discussionsupporting

confidence: 94%

Co-activation of P2Y2 Receptor and TRPV Channel by ATP: Implications for ATP Induced Pain

Lakshmi

Joshi

2005

Cell Mol Neurobiol

View full text Add to dashboard Cite

1. Extracellular ATP is recognized as a peripheral modulator of pain. Activation of ionotropic P2X receptors in sensory neurons has been implicated in induction of pain, whereas metabotropic P2Y receptors in potentiation of pain induced by chemical or physical stimuli via capsaicin sensitive TRPV1 channel. Here we report that P2Y2 receptor activation by ATP can activate the TRPV1 channel in absence of any other stimuli. 2. ATP-induced Ca2+ signaling was studied in Neuro2a cells. ATP evoked release of intracellular Ca2+ from ER and Ca2+ influx through a fast inactivating channel. The Ca2+ response was induced by P2Y receptor agonists in the order of potency ATP>or=UTP>or=ATPgammaS>ADP and was inhibited by suramin and PPADS. The P2X receptor agonist alpha beta methyl ATP was ineffective. 3. The Ca2+ influx was blocked by ruthenium red, an inhibitor of TRPV1 channel. Capsaicin, the most potent activator of the TRPV1 channel, evoked a fast inactivating Ca2+ transient suggesting the presence of endogenous TRPV1 channels in Neuro2a cells. NMS and PDBu, repressors of IP3 formation, drastically inhibited both the components of Ca2+ response. 4. Our data show co-activation of the P2Y2 receptor and capsaicin sensitive TRPV1 channel by ATP. Such functional interaction between endogenous P2Y2 receptor and TRPV1 channels could explain the ATP-induced pain.

show abstract

Section: Discussionsupporting

confidence: 94%

Co-activation of P2Y2 Receptor and TRPV Channel by ATP: Implications for ATP Induced Pain

Lakshmi

Joshi

2005

Cell Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…ATP applied to mouse neuroblastoma Neuro-2A cells resulted in a selective enhancement of plasma membrane permeability for Na + relative to K + , but also inward Cl − pumping [540], probably via P2Y receptors [541]. ATP and UTP were shown to increase [Ca 2+ ] i in the murine neuroblastoma cell line NIE-115 [542], perhaps via P2Y 2 and/or P2Y 4 receptors.…”

Section: Neuroblastoma/neuromamentioning

confidence: 93%

Purinergic signalling and cancer

Burnstock

Virgilio

2013

Purinergic Signalling

266

265

View full text Add to dashboard Cite

Receptors for extracellular nucleotides are widely expressed by mammalian cells. They mediate a large array of responses ranging from growth stimulation to apoptosis, from chemotaxis to cell differentiation and from nociception to cytokine release, as well as neurotransmission. Pharma industry is involved in the development and clinical testing of drugs selectively targeting the different P1 nucleoside and P2 nucleotide receptor subtypes. As described in detail in the present review, P2 receptors are expressed by all tumours, in some cases to a very high level. Activation or inhibition of selected P2 receptor subtypes brings about cancer cell death or growth inhibition. The field has been largely neglected by current research in oncology, yet the evidence presented in this review, most of which is based on in vitro studies, although with a limited amount from in vivo experiments and human studies, warrants further efforts to explore the therapeutic potential of purinoceptor targeting in cancer.

show abstract

“…Coincidently, receptors of many inflammatory mediators are coupled to the very same G q/11 -PLC signalling pathway as the above mentioned M 1 and B 2 receptors; many of these receptors are prominent in peripheral nociceptors and are known to be able to excite them. Among those receptors are the B 2 receptors themselves [151], histamine H1 receptors [152], protease-activated receptor-2 (PAR2) [153], prostaglandin EP1 [154], purinergic P2Y [155] and many other receptors (reviewed in [16]). Accordingly, stimulation of nociceptive neurons by bradykinin (an endogenous peptide that has been called “the most potent endogenous algogenic substance known” [156]) [8, 10] strongly inhibited M current and produced excitability which was mimicked by M channel blocker XE991 and antagonised by M channel enhancer flupirtine.…”

Section: K+ Channels and Inflammatory Painmentioning

confidence: 99%

Potassium Channels in Peripheral Pain Pathways: Expression, Function and Therapeutic Potential

Du¹,

Gamper²

2013

110

103

View full text Add to dashboard Cite

Electrical excitation of peripheral somatosensory nerves is a first step in generation of most pain signals in mammalian nervous system. Such excitation is controlled by an intricate set of ion channels that are coordinated to produce a degree of excitation that is proportional to the strength of the external stimulation. However, in many disease states this coordination is disrupted resulting in deregulated peripheral excitability which, in turn, may underpin pathological pain states (i.e. migraine, neuralgia, neuropathic and inflammatory pains). One of the major groups of ion channels that are essential for controlling neuronal excitability is potassium channel family and, hereby, the focus of this review is on the K+ channels in peripheral pain pathways. The aim of the review is threefold. First, we will discuss current evidence for the expression and functional role of various K+ channels in peripheral nociceptive fibres. Second, we will consider a hypothesis suggesting that reduced functional activity of K+ channels within peripheral nociceptive pathways is a general feature of many types of pain. Third, we will evaluate the perspectives of pharmacological enhancement of K+ channels in nociceptive pathways as a strategy for new analgesic drug design.

show abstract

P2Y Receptor Linked to Phospholipase C: Stimulation of Neuro 2A Cells by UTP and ATP and Possible Regulation by Protein Kinase C Subtype ε

Cited by 20 publications

References 22 publications

Co-activation of P2Y2 Receptor and TRPV Channel by ATP: Implications for ATP Induced Pain

Co-activation of P2Y2 Receptor and TRPV Channel by ATP: Implications for ATP Induced Pain

Purinergic signalling and cancer

Potassium Channels in Peripheral Pain Pathways: Expression, Function and Therapeutic Potential

Contact Info

Product

Resources

About