Differential effects of substance P or hemokinin-1 on transient receptor potential channels, TRPV1, TRPA1 and TRPM8, in the rat

Naono-Nakayama, Rumi; Sunakawa, Natsuki; Ikeda, Tetsuya; Nishimori, Toshikazu

doi:10.1016/j.npep.2009.10.002

Cited by 24 publications

(15 citation statements)

References 30 publications

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“…These data extend the physiological characterization of TRPM8 in mouse sperm (25,27), and in doing so, we have described only the second endogenous protein antagonist of TRPM8 (37). TRPM8 is an outward rectifying cation channel of the TRP family and is permeable to Ca 2+ , Cs + , Na 2+ , and K + .…”

Section: E)supporting

confidence: 72%

Cysteine-rich secretory protein 4 is an inhibitor of transient receptor potential M8 with a role in establishing sperm function

Gibbs¹,

Orta

Reddy³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

110

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The cysteine-rich secretory proteins (CRISPs) are a group of four proteins in the mouse that are expressed abundantly in the male reproductive tract, and to a lesser extent in other tissues. Analysis of reptile CRISPs and mouse CRISP2 has shown that CRISPs can regulate cellular homeostasis via ion channels. With the exception of the ability of CRISP2 to regulate ryanodine receptors, the in vivo targets of mammalian CRISPs function are unknown. In this study, we have characterized the ion channel regulatory activity of epididymal CRISP4 using electrophysiology, cell assays, and mouse models. Through patch-clamping of testicular sperm, the CRISP4 CRISP domain was shown to inhibit the transient receptor potential (TRP) ion channel TRPM8. These data were confirmed using a stably transfected CHO cell line. TRPM8 is a major cold receptor in the body, but is found in other tissues, including the testis and on the tail and head of mouse and human sperm. Functional assays using sperm from wild-type mice showed that TRPM8 activation significantly reduced the number of sperm undergoing the progesteroneinduced acrosome reaction following capacitation, and that this response was reversed by the coaddition of CRISP4. In accordance, sperm from Crisp4 null mice had a compromised ability to undergo to the progesterone-induced acrosome reaction. Collectively, these data identify CRISP4 as an endogenous regulator of TRPM8 with a role in normal sperm function.cysteine-rich secretory proteins | antigen 5 | pathogenesis-related 1 | epididymal maturation | fertility

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Section: E)supporting

confidence: 72%

Cysteine-rich secretory protein 4 is an inhibitor of transient receptor potential M8 with a role in establishing sperm function

Gibbs¹,

Orta

Reddy³

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

110

View full text Add to dashboard Cite

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“…Moreover, as already mentioned, acidification of the external milieu (a known feature of inflammation) also leads to a reduction in TRPM8 activity [66]. At whole animal level, menthol-induced scratching behavior (presumably mediated by TRPM8) was attenuated by intrathecal administration of tachykinins substance P and hemokinin-1, two neuropeptides involved in neurogenic inflammation [89]. Taken together, these results indicate that TRPM8 is inhibited following an acute inflammatory challenge.…”

Section: Inflammationsupporting

confidence: 60%

TRPM8, a Sensor for Mild Cooling in Mammalian Sensory Nerve Endings

Babeș

Ciobanu²,

Neacsu³

et al. 2011

CPB

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Temperature sensing is a crucial feature of the nervous system, enabling organisms to avoid physical danger and choose optimal environments for survival. TRPM8 (Transient Receptor Potential Melastatin type 8) belongs to a select group of ion channels which are gated by changes in temperature, are expressed in sensory nerves and/or skin cells and may be involved in temperature sensing. This channel is activated by a moderate decrease in temperature, with a threshold of approximately 25 °C in heterologous expression systems, and by a variety of natural and synthetic compounds, including menthol. While the physiological role of TRPM8 as a transducer of gentle cooling is widely accepted, its involvement in acute noxious cold sensing in healthy tissues is still under debate. Although accumulating evidence indicates that TRPM8 is involved in neuropathic cold allodynia, in some animal models of nerve injury peripheral and central activation of TRPM8 is followed by analgesia. A variety of inflammatory mediators, including bradykinin and prostaglandin E(2), modulate TRPM8 by inhibiting the channel and shifting its activation threshold to colder temperatures, most likely counteracting the analgesic action of TRPM8. While important progress has been made in unraveling the biophysical features of TRPM8, including the revelation of its voltage dependence, the precise mechanism involved in temperature sensing by this channel is still not completely understood. This article will review the current status of knowledge regarding the (patho)physiological role(s) of TRPM8, its modulation by inflammatory mediators, the signaling pathways involved in this regulation, and the biophysical properties of the channel.

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“…TAC4 mRNA expression is uniform throughout the whole body, and the intact brain also expresses TAC4 mRNA at comparable amounts to peripheral tissues [7]. In addition, many reports have intriguingly indicated differences in the effects of SP and HK-1 [3]–[6], although both peptides activate NK 1 receptors with comparable high affinity and potency and both NK 2 and NK 3 receptors with lower affinities [1], [2]. Therefore, HK-1 may be distinct from SP not only in its expressing cells, but also in its roles in the CNS.…”

Section: Discussionmentioning

confidence: 99%

“…The representative tachykinin peptide, substance P (SP), is encoded by the TAC1 gene and preferentially activates a G-protein-coupled receptor, NK 1 . The most recently identified tachykinin member, hemokinin-1 (HK-1; encoded by the TAC4 gene), also activates the NK 1 receptor with similar affinity and potency to SP [1], [2], although the effects of SP and HK-1 are slightly different [3]–[6]. In addition, the TAC4 and TAC1 expression patterns differ considerably.…”

Section: Introductionmentioning

confidence: 99%

Hemokinin-1 Gene Expression Is Upregulated in Microglia Activated by Lipopolysaccharide through NF-κB and p38 MAPK Signaling Pathways

et al. 2012

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The mammalian tachykinins, substance P (SP) and hemokinin-1 (HK-1), are widely distributed throughout the nervous system and/or peripheral organs, and function as neurotransmitters or chemical modulators by activating their cognate receptor NK1. The TAC1 gene encoding SP is highly expressed in the nervous system, while the TAC4 gene encoding HK-1 is uniformly expressed throughout the body, including a variety of peripheral immune cells. Since TAC4 mRNA is also expressed in microglia, the resident immune cells in the central nervous system, HK-1 may be involved in the inflammatory processes mediated by these cells. In the present study, we found that TAC4, rather than TAC1, was the predominant tachykinin gene expressed in primary cultured microglia. TAC4 mRNA expression was upregulated in the microglia upon their activation by lipopolysaccharide, a well-characterized Toll-like receptor 4 agonist, while TAC1 mRNA expression was downregulated. Furthermore, both nuclear factor-κB and p38 mitogen-activated protein kinase intracellular signaling pathways were required for the upregulation of TAC4 mRNA expression, but not for the downregulation of TAC1 mRNA expression. These findings suggest that HK-1, rather than SP, plays dominant roles in the pathological conditions associated with microglial activation, such as neurodegenerative and neuroinflammatory disorders.

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Differential effects of substance P or hemokinin-1 on transient receptor potential channels, TRPV1, TRPA1 and TRPM8, in the rat

Cited by 24 publications

References 30 publications

Cysteine-rich secretory protein 4 is an inhibitor of transient receptor potential M8 with a role in establishing sperm function

Cysteine-rich secretory protein 4 is an inhibitor of transient receptor potential M8 with a role in establishing sperm function

TRPM8, a Sensor for Mild Cooling in Mammalian Sensory Nerve Endings

Hemokinin-1 Gene Expression Is Upregulated in Microglia Activated by Lipopolysaccharide through NF-κB and p38 MAPK Signaling Pathways

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