2017
DOI: 10.1016/j.expneurol.2017.06.007
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Regulation of transient receptor potential cation channel subfamily V1 protein synthesis by the phosphoinositide 3-kinase/Akt pathway in colonic hypersensitivity

Abstract: The transient receptor potential cation channel subfamily V member 1 (TRPV1), also known as the capsaicin receptor or vanilloid receptor 1 (VR1), is expressed in nociceptive neurons in the dorsal root ganglia (DRG) and participates in the transmission of pain. The present study investigated the underlying molecular mechanisms by which TRPV1 was regulated by nerve growth factor (NGF) signaling pathways in colonic hypersensitivity in response to colitis. We found that during colitis TRPV1 protein levels were sig… Show more

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Cited by 27 publications
(32 citation statements)
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References 56 publications
(112 reference statements)
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“…Enhancing the activity of pronociceptive receptors and/or ion channels on primary afferent neurons can result in sensory hypersensitivity. NGF increases the transient receptor potential cation channel subfamily V1 (TRPV1) expression in DRG . TRPV1 is a nonselective cation channel that mediates scalding heat and pain.…”
Section: Neurotrophic Factors and Visceral Sensitivitymentioning
confidence: 99%
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“…Enhancing the activity of pronociceptive receptors and/or ion channels on primary afferent neurons can result in sensory hypersensitivity. NGF increases the transient receptor potential cation channel subfamily V1 (TRPV1) expression in DRG . TRPV1 is a nonselective cation channel that mediates scalding heat and pain.…”
Section: Neurotrophic Factors and Visceral Sensitivitymentioning
confidence: 99%
“…TRPV1 is a nonselective cation channel that mediates scalding heat and pain. Upregulation of TRPV1 by NGF via the phosphoinositide 3‐kinase (PI3K)/Akt pathway may contribute to visceral hypersensitivity following TNBS‐induced colitis . Mechanical stretch in bowel obstruction causes upregulation of NGF in gut smooth muscle cells .…”
Section: Neurotrophic Factors and Visceral Sensitivitymentioning
confidence: 99%
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“…Activation of mature astrocytes is mainly manifested as enhanced GFAP expression which is necessary for the completion of gliosis of reactive astrocytes. Intestinal inflammation injury leads to the activation of spinal cord astrocytes which release a large number of neuroactive substances, enhance the sensitivity and reactivity of dorsal horn neurons, and generate central sensitization [15,16]. For example, 2,4,6-trinitrobenzene sulfonic acid (TNBS) can lead to the enhancement of long-term potentiation (LTP) in pain synaptic transmission of the spinal dorsal horn in colitis rats [17].…”
Section: Introductionmentioning
confidence: 99%