Contribution of TRPV1 to Microglia-Derived IL-6 and NFκB Translocation with Elevated Hydrostatic Pressure

Sappington, Rebecca M.; Calkins, David J.

doi:10.1167/iovs.07-1355

Cited by 132 publications

(126 citation statements)

References 114 publications

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“…Once released, these neuropeptides bind to their receptors on neurons and glia and trigger downstream signaling events leading to central sensitization [12][13][14][15][16][17][18][19][20][21][22]. Neuronal activity increases endovanilloid levels during chronic pain conditions, which are synthesized and released on demand [42][43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

“…It is likely that peripheral injury-induced neuronal activity releases Calcitonin GeneRelated Peptide (CGRP) and Substance P (SP) from presynaptic nerve terminals and activation of glia influencing the synthesis and release of anandamide and proand anti-inflammatory mediators. Anandamide and inflammatory mediators act retrogradely to modulate synaptic transmission and TRPV1 expression and function, respectively [12][13][14][15][16][17][18][19][20][21][22]. Resiniferatoxin (RTX) is an ultrapotent TRPV1 agonist, which activates TRPV1 in an irreversible manner.…”

Section: Transient Receptor Potential Vanilloid 1 (Trpv1) Is a Camentioning

confidence: 99%

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Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Yu¹,

Premkumar²

2015

TOPAINJ

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Transient Receptor Potential Vanilloid 1 (TRPV1) expressed in peripheral terminals is responsible for transducing thermal and chemical nociception. Role of TRPV1 expressed in the central terminals is not clear, however, its activation modulates synaptic transmission and contributes to central sensitization. In this study, we have determined the role of TRPV1 expressed in the peripheral and central terminals using resiniferatoxin (RTX), a potent TRPV1 agonist. A single intraplantar injection of RTX, within two days induced loss of capsaicin-induced nocifensive behavior and enhanced response latency to hot plate, which recovered over a period of two months. RTX treatment resulted in the ablation of peripheral TRPV1 expressing fibers in paw skin, which regenerated over the same time period. On the other hand, a single dose of intrathecal administration of RTX, within two days caused thermal hypoalgesia. RTX treatment ablated TRPV1 expressing central sensory nerve terminals. Intriguingly, in contrast to peripheral nerve terminal regeneration that occurred within two months, the central TRPV1 expressing nerve terminals did not regenerate even after five months. The present study demonstrates that TRPV1 in the peripheral and central terminals play a role in nociception and the peripheral terminals have the ability to regenerate, whereas the central terminals do not regenerate even after five months.

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Section: Discussionmentioning

confidence: 99%

Section: Transient Receptor Potential Vanilloid 1 (Trpv1) Is a Camentioning

confidence: 99%

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Yu¹,

Premkumar²

2015

TOPAINJ

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“…50) In this context, in an experimental model of Parkinson's disease, the TRPV1 selective agonist capsaicin inhibits microglia-mediated ROS production, leading to the resultant blockade of the death of dopaminergic neurons. 51) Moreover, TRPV1 partially regulates cytokine production induced by elevated hydrostatic pressure in retinal microglia. 52) Further investigations are warranted to clarify the pathophysiological roles of microglial TRPV1 in CNS diseases.…”

Section: Physiological and Pathophysiological Roles Of Trpv Channels mentioning

confidence: 99%

Physiological and Pathophysiological Roles of Transient Receptor Potential Channels in Microglia-Related CNS Inflammatory Diseases

Shirakawa

Kaneko

2018

Biological & Pharmaceutical Bulletin

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Central nervous system (CNS) inflammation is a potential therapeutic target for neurodegenerative diseases. In recent years, a number of studies have focused on the links between neurodegenerative diseases and CNS glial cells, especially microglia. Microglia are the main resident immune cells in the CNS and represent approximately 10-15% of all CNS cells. Microglia play an important role in maintaining brain homeostasis at rest by surveying the environment, and engulfing apoptotic cells and debris in the healthy brain. However, under certain pathological conditions, microglia can generate neurotoxic factors, such as pro-inflammatory cytokines and molecules like nitric oxide (NO), which lead to CNS inflammatory diseases. In this review, we discuss the evidence that regulation of microglial ion channels may modulate CNS inflammation and subsequent tissue damage in neurological disorders. In particular, we discuss the role of transient receptor potential (TRP) channels in microglia in both acute and chronic inflammatory conditions, and describe the physiological and pathophysiological roles of TRP channels in CNS inflammatory pathways. Additionally, we describe the benefits of stimulation/inhibition of TRP channels in animal models of microglia-related CNS inflammatory diseases.

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“…TRPV1, TRPV2, TRPV3 and TRPV4 channels are expressed in the cornea whereas TRPV1, TRPV2, TRPV5 and TRPV6 channels are expressed in the retina. [15][16][17][18][19][20] The TRPA channel subfamily has only one member, TRPA1. Fig.…”

Section: Wwwintechopencommentioning

confidence: 99%

Transient Receptor Potential (TRP) Channels in the Eye

Pan¹,

Capó-Aponte²,

Reinach³

2012

Advances in Ophthalmology

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Contribution of TRPV1 to Microglia-Derived IL-6 and NFκB Translocation with Elevated Hydrostatic Pressure

Abstract: Elevated pressure induces an influx of extracellular Ca(2+) in retinal microglia that precedes the activation of NFkappaB and the subsequent production and release of IL-6 and is at least partially dependent on the activation of TRPV1 and other ruthenium red-sensitive channels.

Cited by 132 publications

References 114 publications

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Ablation and Regeneration of Peripheral and Central TRPV1 Expressing Nerve Terminals and the Consequence of Nociception

Physiological and Pathophysiological Roles of Transient Receptor Potential Channels in Microglia-Related CNS Inflammatory Diseases

Transient Receptor Potential (TRP) Channels in the Eye

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