ArticleJournal of molecular neuroscience : MN2007
Nitric oxide-NGF mediated PPTA/SP, ADNP, and VIP expression in the peripheral nervous system.
Article in Journal of molecular neuroscience : MN, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Axonal motor polyneuropathy in a 13 years old Girl with a de Novo variant in ADNP.Neurogenetics · 2025Article
- Article
- The Neuroimmune Axis in Skin Sensation, Inflammation, and Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
- Seizure-induced oxidative stress in temporal lobe epilepsy.BioMed research international · 2015Review
- Differential regulation of vasoactive intestinal peptide (VIP) in the dentate gyrus and hippocampus via the NO-cGMP pathway following kainic acid-induced seizure in the rat.Journal of molecular neuroscience : MN · 2010Article
- Nitric oxide regulates activity-dependent neuroprotective protein (ADNP) in the dentate gyrus of the rodent model of kainic acid-induced seizure.Journal of molecular neuroscience : MN · 2009Article
- Neuroprotective protein and carboxypeptidase E.Journal of molecular neuroscience : MN · 2009Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Nerve growth factor (NGF)-deprivation or axotomy of dorsal root ganglion (DRG) neurons causes stress, which they cope by triggering various mechanisms. Among several molecular changes, in the present study, we demonstrate preprotachykinin-A-substance P (PPTA-SP) and activity-dependent neuroprotective protein-vasoactive intestinal peptide (ADNP-VIP) expression pattern using DRG neurons-Schwann cells coculture and axotomy model. In the presence of NGF, DRG cultures showed high levels of PPTA and ADNP mRNA expression, which were significantly suppressed in the absence of NGF and/or nitric oxide synthase (NOS) inhibition by NG-nitro-L-arginine methyl ester (L-NAME), suggesting that both NGF and nitric oxide (NO) can regulate PPTA and ADNP expression. However, treating coculture with NO donor, diethylenetriamine nitric oxide (DETA-NO) did not increase PPTA and ADNP expression in the presence or absence of NGF, although there was a marginal increase in ADNP expression in the absence of NGF. NGF-deprivation increases endogenous NO; thus, DETA-NO had no further effect on PPTA and ADNP expression. Alternatively, NGF produced from NO-stimulated Schwann cells influence gene expression. In addition, interestingly, DETA-NO treatment of Schwann cells alone suppresses both PPTA and ADNP, suggesting differential response of DRG neurons-Schwann cells coculture to DETA-NO. SP and ADNP immunostaining of axotomized DRGs revealed significant reduction in SP and ADNP compared to intact DRG, which was partially recovered in neuronal NOS blocker, 7-nitroindazole (7-NI)-treated DRGs, particularly intense ADNP staining in satellite glia. As ADNP is VIP-responsive gene, we further explored VIP expression in DRGs. Axotomy increased VIP in DRG neurons, but 7-NI treatment caused intense VIP staining in satellite glia. These observations suggest a complex interaction of NO-NGF with PPTA/SP and ADNP-VIP in neuron-glial communication when neurons are stressed.
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