Davidson, Scott

Lear, Marissa

MacKenzie, Alasdair

Ross, Ruth Alexandra

Shanley, Lynne

Journal of Neuroinflammation

English

PubMed

Aberdeen University Research

A: Long-Range Regulatory Synergy Is Required to Allow Control of the TAC1 Locus by MEK/ERK Signalling in Sensory Neurones. Neurosignals

A: Substance P expression in TRPV1 and trkApositive dorsal root ganglion neurons innervating the mouse lung. Respir Physiol Neurobiol

Airway smooth muscle cells express functional neurokinin-1 receptors and the nerve-derived preprotachykinin-a gene: regulation by passive sensitization.

al: Regulation and role of REST and REST4 variants in modulation of gene expression in in vivo and in vitro in epilepsy models. Neurobiol Dis

BN: Substance P and neurokinin-1 receptor expression by intrinsic airway neurons in the rat. Am J Physiol Lung Cell Mol Physiol

Cervero F: Role of central and peripheral tachykinin NK1 receptors in capsaicin- induced pain and hyperalgesia in mice. Pain

CJ: Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons. Nature

et al: Elliptic flow in Au +Au collisions at square root(S)NN = 130 GeV. Phys Rev Lett

Expression of tachykinin receptors inXenopus oocytes injected with poly (A)(+) RNA from cat dorsal root ganglion. Sci China C Life Sci

F: The role of substance P in inflammatory disease.

Gontijo JA: Expression and localization of NK(1)R, substance P and CGRP are altered in dorsal root ganglia neurons of spontaneously hypertensive rats (SHR). Brain Res Mol Brain Res

HG: Prostaglandin E2 increases the expression of the neurokinin1 receptor in adult sensory neurones in culture: a novel role of prostaglandins.

Inflammatory mediators modulating the transient receptor potential vanilloid 1 receptor: therapeutic targets to treat inflammatory and neuropathic pain. Expert Opin Ther Targets

JE: NK-1 and NK-3 type tachykinin receptor mRNA expression in the rat spinal cord dorsal horn is increased during adjuvant or formalin- induced nociception.

JL: Nociceptive response to innocuous mechanical stimulation is mediated via myelinated afferents and NK-1 receptor activation in a rat model of neuropathic pain. Exp Neurol

JP: The rat preprotachykinin-A promoter is regulated in PC12 cells by the synergistic action of multiple stimuli.

JV: Immunohistochemical co-localization of transient receptor potential vanilloid (TRPV)1 and sensory neuropeptides in the guinea-pig respiratory system. Neuroscience

Krause JE: Effects of systemic resiniferatoxin treatment on substance P mRNA in rat dorsal root ganglia and substance P receptor mRNA in the spinal dorsal horn. Brain Res

Mezey E: Hypoalgesia in mice with a targeted deletion of the tachykinin 1 gene. Proc Natl Acad Sci USA

Molecular mechanisms of neuropathic pain-phenotypic switch and initiation mechanisms. Pharmacol Ther

Neuron restrictive silencer factor as a modulator of neuropeptide gene expression. Regul Pept

Neuropeptide expression by newborn and adult rat sensory neurons in culture: effects of nerve growth factor and other neurotrophic factors. Neuroscience

Nuclear factor-kappaB accounts for the repressor effects of high stromal cell-derived factor-1alpha levels on Tac1 expression in nontumorigenic breast cells. Mol Cancer Res

Pauwels RA: Presence of substance P and neurokinin 1 receptors in human sputum macrophages and U-937 cells. Eur Respir J

Presence of substance P and the neurokinin-1 receptor in tenocytes of the human Achilles tendon. Regul Pept

Role of preprotachykinin-A gene products on multiple organ injury in LPS-induced endotoxemia.

Seckl JR: Neuropeptide gene expression and capsaicin-sensitive primary afferents: maintenance and spread of adjuvant arthritis in the rat.

Substance P content and preprotachykinin gene-I mRNA expression in a rat model of chronic bronchitis.

Substance P induced by peripheral nerve injury in primary afferent sensory neurons and its effect on dorsal column nucleus neurons.

Substance P: a pioneer amongst neuropeptides.

T: TRPV1: on the road to pain relief. Curr Mol Pharmacol

Targeting bacterial endotoxin: two sides of a coin.

Todorovic SM, Arneric SP, Snutch TP: Role of voltage-gated calcium channels in ascending pain pathways. Brain Res Rev

Toll-like receptor 4 in CNS pathologies.

Tomlinson DR: Effect of capsaicin on substance P and nerve growth factor in adjuvant arthritic rats. Neurosci Lett

TW: Chimeric NK1 (substance P)/NK3 (neurokinin B) receptors. Identification of domains determining the binding specificity of tachykinin agonists.

YL: Lipopolysaccharide induces preprotachykinin gene expression.

Zhao ZQ: Neurokinin-1 receptor enhances TRPV1 activity in primary sensory neurons via PKCepsilon: a novel pathway for heat hyperalgesia.

Evidence for regulatory diversity and auto-regulation at the TAC1 locus in sensory neurones

Abstract
          The neuropeptide substance-P (SP) is expressed from the TAC1 gene in sensory neurones where it acts as a key modulator of neurogenic inflammation. The promoter of TAC1 (TAC1prom) plays a central role in the regulation of the TAC1 gene but requires the presence of a second regulatory element; ECR2, to support TAC1 expression in sensory neurones and to respond appropriately to signalling pathways such as MAPkinases and noxious induction by capsaicin. We examined whether the effect of capsaicin on ECR2-TAC1prom activity in larger diameter neurones was cell autonomous or non- cell autonomous. We demonstrate that TRPV1 is not expressed in all the same cells as SP following capsaicin induction suggesting the presence of a non-cell autonomous mechanism for TAC1 up-regulation following capsaicin induction. In addition, we demonstrate that induction of SP and ECR1-TAC1prom activity in these larger diameter neurones can be induced by potassium depolarisation suggesting that, in addition to capsaicin induction, transgene activity may be modulated by voltage gated calcium channels. Furthermore, we show that NK1 is expressed in all SP- expressing cells after capsaicin induction and that an agonist of NK1 can activate both SP and the transgene in larger diameter neurones. These observations suggest the presence of an autocrine loop that controls the expression of the TAC1 promoter in sensory neurones. In contrast, induction of the TAC1 promoter by LPS was not dependent on ECR2 and did not occur in large diameter neurones. These studies demonstrate the diversity of mechanisms modulating the activity of the TAC1 promoter and provide novel directions for the development of new anti-inflammatory therapies.</jats:p

Lynne Shanley

Marissa Lear

Scott Davidson

Ruth Ross

Alasdair MacKenzie

Crossref

Springer - Publisher Connector

Abstract The neuropeptide substance-P (SP) is expressed from the TAC1 gene in sensory neurones where it acts as a key modulator of neurogenic inflammation. The promoter of TAC1 (TAC1prom) plays a central role in the regulation of the TAC1 gene but requires the presence of a second regulatory element; ECR2, to support TAC1 expression in sensory neurones and to respond appropriately to signalling pathways such as MAPkinases and noxious induction by capsaicin. We examined whether the effect of capsaicin on ECR2-TAC1prom activity in larger diameter neurones was cell autonomous or non- cell autonomous. We demonstrate that TRPV1 is not expressed in all the same cells as SP following capsaicin induction suggesting the presence of a non-cell autonomous mechanism for TAC1 up-regulation following capsaicin induction. In addition, we demonstrate that induction of SP and ECR1-TAC1prom activity in these larger diameter neurones can be induced by potassium depolarisation suggesting that, in addition to capsaicin induction, transgene activity may be modulated by voltage gated calcium channels. Furthermore, we show that NK1 is expressed in all SP- expressing cells after capsaicin induction and that an agonist of NK1 can activate both SP and the transgene in larger diameter neurones. These observations suggest the presence of an autocrine loop that controls the expression of the TAC1 promoter in sensory neurones. In contrast, induction of the TAC1 promoter by LPS was not dependent on ECR2 and did not occur in large diameter neurones. These studies demonstrate the diversity of mechanisms modulating the activity of the TAC1 promoter and provide novel directions for the development of new anti-inflammatory therapies.</p

Ross Ruth

Davidson Scott

Lear Marissa

Shanley Lynne

MacKenzie Alasdair

Directory of Open Access Journals

A noxious stimulus induces the preprotachykinin-A gene expression in the rat dorsal root ganglion: a quantitative study using in situ hybridization histochemistry. Brain Res

Ca2+ channel currents in rat sensory neurones: interaction between guanine nucleotides, cyclic AMP and Ca2+ channel ligands.

Extensive regeneration in vitro by early embryonic neurons on immature and adult CNS tissue.

not PKG mediate LPS-induced CGRP release and [Ca(2+)](i) elevation in DRG neurons of neonatal rats.

PF: Chronic treatment with nicotine or potassium attenuates depolarisation-evoked noradrenaline release from the human neuroblastoma SH-SY5Y. Neurosci Lett

PS: LPS/TLR4 signal transduction pathway. Cytokine

SB: Abnormal substance P release from the spinal cord following injury to primary sensory neurons.

Seckl JR: Adjuvant-induced joint inflammation causes very rapid transcription of beta- preprotachykinin and alpha-CGRP genes in innervating sensory ganglia.

Similar and different effects of capsaicin and resiniferatoxin on substance P release and transient receptor potential vanilloid type 1 expression of cultured rat dorsal root ganglion neurons. Methods Find Exp Clin Pharmacol

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Evidence for regulatory diversity and auto-regulation at the TAC1 locus in sensory neurones

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