ArticleInternational journal of molecular sciences2024
Nerve Growth Factor Signaling Modulates the Expression of Glutaminase in Dorsal Root Ganglion Neurons during Peripheral Inflammation.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Cdk5 regulates glutamine metabolism in colorectal cancer via the EZH2-GLS1 axis.Cancer & metabolism · 2025Article
- A process optimization and release modeling of coaxial electrospun aligned core-shell poly (ethylene oxide-poly(l-lactide-co-glycolide)) nanofibers encapsulating nerve growth factor.Journal of applied polymer science · 2025Article
- Loss of Glutaminase 1 in Small Sensory Neurons Prevents Nerve Injury Induced Mechanical Allodynia: Insights From Conditional Knockout Mice.European journal of pain (London, England) · 2025Article
- NGF in Neuropathic Pain: Understanding Its Role and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
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Authors and funding
4 authors.
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Abstract
Glutamate functions as the major excitatory neurotransmitter for primary sensory neurons and has a crucial role in sensitizing peripheral nociceptor terminals producing sensitization. Glutaminase (GLS) is the synthetic enzyme that converts glutamine to glutamate. GLS-immunoreactivity (-ir) and enzyme activity are elevated in dorsal root ganglion (DRG) neuronal cell bodies during chronic peripheral inflammation, but the mechanism for this GLS elevation is yet to be fully characterized. It has been well established that, after nerve growth factor (NGF) binds to its high-affinity receptor tropomyosin receptor kinase A (TrkA), a retrograde signaling endosome is formed. This endosome contains the late endosomal marker Rab7GTPase and is retrogradely transported via axons to the cell soma located in the DRG. This complex is responsible for regulating the transcription of several critical nociceptive genes. Here, we show that this retrograde NGF signaling mediates the expression of GLS in DRG neurons during the process of peripheral inflammation. We disrupted the normal NGF/TrkA signaling in adjuvant-induced arthritic (AIA) Sprague Dawley rats by the pharmacological inhibition of TrkA or blockade of Rab7GTPase, which significantly attenuated the expression of GLS in DRG cell bodies. The results indicate that NGF/TrkA signaling is crucial for the production of glutamate and has a vital role in the development of neurogenic inflammation. In addition, our pain behavioral data suggest that Rab7GTPase can be a potential target for attenuating peripheral inflammatory pain.
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