ArticleInternational journal of molecular sciences2017
ProNGF, but Not NGF, Switches from Neurotrophic to Apoptotic Activity in Response to Reductions in TrkA Receptor Levels.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 90 citations in OpenAlex.
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- A neurotrophic withdrawal hypothesis for multisystem adverse events associated with anti-NGF therapy for canine osteoarthritis pain.Frontiers in veterinary science · 2026Article
- Nerve growth factor responsive elements modulate immune cell inflammation and are dysregulated in an Alzheimer's disease mouse model.Frontiers in immunology · 2026Article
- Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases.Experimental neurobiology · 2025Review
- Tissue Expression of NGF in Skin Lesions of HIV-Coinfected and Non-Coinfected Leprosy Patients and Its Relationship with Leprosy Neural Damage.Microorganisms · 2025Article
- Cholinotrophic basal forebrain connectome dysfunction in Down syndrome with and without dementia.iScience · 2025Article
- Bladder p75Life (Basel, Switzerland) · 2025Article
- Elevated NGF provokes decidual lipid peroxidation and promotes preterm birth in mice.Journal of translational medicine · 2025Article
- Delivery of Neuroregenerative Proteins to the Brain for Treatments of Neurodegenerative Brain Diseases.Life (Basel, Switzerland) · 2024Review
- Phytotherapeutic BS012 and Its Active Component Ameliorate Allergic Asthma via Inhibition of Th2-Mediated Immune Response and Apoptosis.Biomolecules & therapeutics · 2024Article
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- Sortilin is dispensable for secondary injury processes following traumatic brain injury in mice.Heliyon · 2024Article
- 1953-2023. Seventy Years of the Nerve Growth Factor: A Potential Novel Treatment in Neurological Diseases?Aging and disease · 2024Review
- The expression system affects the binding affinity between p75NTR and proNGF.Biochemistry and biophysics reports · 2024Article
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- Modulation of the p75NTR during Adolescent Alcohol Exposure Prevents Cholinergic Neuronal Atrophy and Associated Acetylcholine Activity and Behavioral Dysfunction.International journal of molecular sciences · 2024Article
- Exploring CNS Involvement in Pain Insensitivity in Hereditary Sensory and Autonomic Neuropathy Type 4: Insights from Tc-99m ECD SPECT Imaging.Tomography (Ann Arbor, Mich.) · 2023Article
- Enhancement of neural regeneration as a therapeutic strategy for Alzheimer's disease (Review).Experimental and therapeutic medicine · 2023Review
- Analysis of β-nerve growth factor and its precursor during human pregnancy by immunoaffinity-liquid chromatography tandem mass spectrometry.Scientific reports · 2023Article
- Decrease in the Ratio proBDNF/BDNF in the Urine of Aging Female Patients with OAB.Metabolites · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nerve growth factor (NGF) promotes the survival and differentiation of neurons. NGF is initially synthesized as a precursor, proNGF, which is the predominant form in the central nervous system. NGF and proNGF bind to TrkA/p75NTR to mediate cell survival and to sortilin/p75NTR to promote apoptosis. The ratio of TrkA to p75NTR affects whether proNGF and mature NGF signal cell survival or apoptosis. The purpose of this study was to determine whether the loss of TrkA influences p75NTR or sortilin expression levels, and to establish whether proNGF and mature NGF have a similar ability to switch between cell survival and cell death. We systematically altered TrkA receptor levels by priming cells with NGF, using small interfering RNA, and using the mutagenized PC12nnr5 cell line. We found that both NGF and proNGF can support cell survival in cells expressing TrkA, even in the presence of p75NTR and sortilin. However, when TrkA is reduced, proNGF signals cell death, while NGF exhibits no activity. In the absence of TrkA, proNGF-induced cell death occurs, even when p75NTR and sortilin levels are reduced. These results show that proNGF can switch between neurotrophic and apoptotic activity in response to changes in TrkA receptor levels, whereas mature NGF cannot. These results also support the model that proNGF is neurotrophic under normal circumstances, but that a loss in TrkA in the presence of p75NTR and sortilin, as occurs in neurodegenerative disease or injury, shifts proNGF, but not NGF, signalling from cell survival to cell death.
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