ArticleJournal of cellular and molecular medicine2008
Nerve growth factor blocks thapsigargin-induced apoptosis at the level of the mitochondrion via regulation of Bim.
Article in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Nerve Growth Factor Treatment and the Corneal Epithelium: Extracellular Vesicle-Mediated Signaling.Journal of extracellular biology · 2026Article
- Baicalein-mediated regulation of Nrf2/ARE, NFĸB, and MAPK signaling in Huntington's disease: a promising strategy against neuroinflammation and neurodegeneration.Inflammopharmacology · 2025Review
- Gambogic amide inhibits angiogenesis by suppressing VEGF/VEGFR2 in endothelial cells in a TrkA-independent manner.Pharmaceutical biology · 2021Article
- Inherited cataracts: Genetic mechanisms and pathways new and old.Experimental eye research · 2021Review
- NGF mediates protection of mesenchymal stem cells-conditioned medium against 2,5-hexanedione-induced apoptosis of VSC4.1 cells via Akt/Bad pathway.Molecular and cellular biochemistry · 2020Article
- Biology of Inherited Cataracts and Opportunities for Treatment.Annual review of vision science · 2019Review
- Long non-coding RNA and microRNA-675/let-7a mediates the protective effect of melatonin against early brain injury after subarachnoid hemorrhage via targeting TP53 and neural growth factor.Cell death & disease · 2018Article
- HSPB1 facilitates ERK-mediated phosphorylation and degradation of BIM to attenuate endoplasmic reticulum stress-induced apoptosis.Cell death & disease · 2017Article
- Mutations and mechanisms in congenital and age-related cataracts.Experimental eye research · 2017Review
- Gelatin Nanostructured Lipid Carriers Incorporating Nerve Growth Factor Inhibit Endoplasmic Reticulum Stress-Induced Apoptosis and Improve Recovery in Spinal Cord Injury.Molecular neurobiology · 2016Article
- Human βA3/A1-crystallin splicing mutation causes cataracts by activating the unfolded protein response and inducing apoptosis in differentiating lens fiber cells.Biochimica et biophysica acta · 2016Article
- Nerve growth factor improves functional recovery by inhibiting endoplasmic reticulum stress-induced neuronal apoptosis in rats with spinal cord injury.Journal of translational medicine · 2014Article
- Nerve growth factor-mediated inhibition of apoptosis post-caspase activation is due to removal of active caspase-3 in a lysosome-dependent manner.Cell death & disease · 2014Article
- Heat shock preconditioning protects against ER stress-induced apoptosis through the regulation of the BH3-only protein BIM.FEBS open bio · 2014Article
- Exogenous basic fibroblast growth factor inhibits ER stress-induced apoptosis and improves recovery from spinal cord injury.CNS neuroscience & therapeutics · 2013Article
- Perk-dependent repression of miR-106b-25 cluster is required for ER stress-induced apoptosis.Cell death & disease · 2012Article
- Kinetics in signal transduction pathways involving promiscuous oligomerizing receptors can be determined by receptor specificity: apoptosis induction by TRAIL.Molecular & cellular proteomics : MCP · 2012Article
- Nerve growth factor in cancer cell death and survival.Cancers · 2011Article
- Early growth response-1 is a regulator of DR5-induced apoptosis in colon cancer cells.British journal of cancer · 2010Article
- Inhibition by anandamide of 6-hydroxydopamine-induced cell death in PC12 cells.International journal of cell biology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined how the neurotrophin, nerve growth factor (NGF), protects PC12 cells against endoplasmic reticulum (ER) stress-induced apoptosis. ER stress was induced using thapsigargin (TG) that inhibits the sarcoplasmic/ER Ca2+-ATPase pump (SERCA) and depletes ER Ca2+ stores. NGF pre-treatment inhibited translocation of Bax to the mitochondria, loss of mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-3, -7 and -9) and apoptosis induction by TG. Notably, TG also caused a marked induction of BimEL mRNA and protein, and knockdown of Bim with siRNA protected cells against TG-induced apoptosis. NGF delayed the induction and increased the phosphorylation of BimEL. NGF-mediated protection was dependent on phosphatidylinositol-3 kinase (PI3K) signalling since all above apoptotic events, including expression and phosphorylation status of BimEL protein, could be reverted by the PI3K inhibitor LY294002. In contrast, NGF had no effect on the TG-mediated induction of the unfolded protein response (increased expression of Grp78, GADD34, splicing of XBP1 mRNA) or ER stress-associated pro-apoptotic responses (induction of C/EBP homologous protein [CHOP], induction and processing of caspase-12). These data indicate that NGF-mediated protection against ER stress-induced apoptosis occurs at the level of the mitochondria by regulating induction and activation of Bim and mitochondrial translocation of Bax.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.