ArticleExperimental neurology2017
Regulation of transient receptor potential cation channel subfamily V1 protein synthesis by the phosphoinositide 3-kinase/Akt pathway in colonic hypersensitivity.
Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- The Role of TRP Channels in Colitis and Inflammatory Bowel Disease: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Transient receptor potential vanilloid channels in inflammatory bowel diseases: linking inflammation, angiogenesis, and oxidative stress.Inflammopharmacology · 2026Review
- Article
- Attenuation of Colitis-Induced Visceral Hypersensitivity and Pain by Selective Silencing of TRPV1-Expressing Fibers in Rat Colon.Inflammatory bowel diseases · 2024Article
- PIK3CA mutations enhance the adipogenesis of ADSCs in facial infiltrating lipomatosis through TRPV1.iScience · 2024Article
- Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization.The Journal of pharmacology and experimental therapeutics · 2024Review
- Opposite effects of acute and chronic IGF1 on rat dorsal root ganglion neuron excitability.Frontiers in cellular neuroscience · 2024Article
- TrkA inhibition alleviates bladder overactivity in cyclophosphamide-induced cystitis by targeting hyperpolarization-activated cyclic nucleotide-gated channels.Iranian journal of basic medical sciences · 2023Article
- Inhibitions and Down-Regulation of Motor Protein Eg5 Expression in Primary Sensory Neurons Reveal a Novel Therapeutic Target for Pathological Pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Transient receptor potential vanilloid type-1 regulates periodontal disease damage via the PI3K/AKT signaling pathway.Iranian journal of basic medical sciences · 2022Article
- Targeting Vascular endothelial growth factor A with soluble vascular endothelial growth factor receptor 1 ameliorates nerve injury-induced neuropathic pain.Molecular pain · 2022Article
- Neuroimmune Interaction: A Widespread Mutual Regulation and the Weapons for Barrier Organs.Frontiers in cell and developmental biology · 2022Review
- Identification of potential biomarkers for abdominal pain in IBS patients by bioinformatics approach.BMC gastroenterology · 2021Article
- Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Article
- Electroacupuncture Inhibits the Activity of Astrocytes in Spinal Cord in Rats with Visceral Hypersensitivity by Inhibiting P2YEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Is TRPA1International journal of molecular sciences · 2019Review
- Neurotrophic factors in enteric physiology and pathophysiology.Neurogastroenterology and motility · 2018Review
- Urinary bladder organ hypertrophy is partially regulated by Akt1-mediated protein synthesis pathway.Life sciences · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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 significantly increased in specifically labeled colonic afferent neurons in both L1 and S1 DRGs. TRPV1 protein up-regulation in DRG was also enhanced by NGF treatment. We then found that TRPV1 protein up-regulation in DRG was regulated by activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway both in vivo and in vitro. Suppression of endogenous PI3K/Akt activity during colitis or NGF treatment with a specific PI3K inhibitor LY294002 reduced TRPV1 protein production in DRG neurons, and also reduced colitis-evoked TRPV1-mediated visceral hypersensitivity tested by hyper-responsiveness to colorectal distention (CRD) and von Frey filament stimulation of abdomen. Further studies showed that TRPV1 mRNA levels in the DRG were not regulated by either colitis or NGF. We then found that an up-regulation of the protein synthesis pathway was involved by which both colitis and NGF caused a PI3K-dependent increase in the phosphorylation level of eukaryotic translation initiation factor 4E-binding protein (4E-BP)1. These results suggest a novel mechanism in colonic hypersensitivity which involves PI3K/Akt-mediated TRPV1 protein, not mRNA, up-regulation in primary afferent neurons, likely through activation of the protein synthesis pathways.
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Registered trials
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