ArticleThe Journal of cell biology2005
Inhibition of NGF deprivation-induced death by low oxygen involves suppression of BIMEL and activation of HIF-1.
Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Sympathetic Nerve Activity and Blood Pressure Response to Exercise in Peripheral Artery Disease: From Molecular Mechanisms, Human Studies, to Intervention Strategy Development.International journal of molecular sciences · 2022Review
- HIF-1α inhibition alleviates the exaggerated exercise pressor reflex in rats with peripheral artery disease induced by femoral artery occlusion.Physiological reports · 2021Article
- EglN3 hydroxylase stabilizes BIM-EL linking VHL type 2C mutations to pheochromocytoma pathogenesis and chemotherapy resistance.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Bax and caspases regulate increased production of mitochondria-derived reactive species in neuronal apoptosis: LACK of A role for depletion of cytochrome c from the mitochondrial electron transport chain.Biochemistry and biophysics reports · 2015Article
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- Sevoflurane Post-conditioning Protects Primary Rat Cortical Neurons Against Oxygen-Glucose Deprivation/Resuscitation: Roles of Extracellular Signal-Regulated Kinase 1/2 and Bid, Bim, Puma.Neurochemical research · 2015Article
- Depletion of PHD3 protects heart from ischemia/reperfusion injury by inhibiting cardiomyocyte apoptosis.Journal of molecular and cellular cardiology · 2015Article
- Tax contributes apoptosis resistance to HTLV-1-infected T cells via suppression of Bid and Bim expression.Cell death & disease · 2014Article
- Gingerol prevents prion protein-mediated neuronal toxicity by regulating HIF prolyl hydroxylase 2 and prion protein.International journal of molecular medicine · 2014Article
- Nerve Growth Factor, Muscle Afferent Receptors and Autonomic Responsiveness with Femoral Artery Occlusion.Journal of modern physiological research · 2014Article
- Femoral Artery Occlusion Increases Muscle Pressor Reflex and Expression of Hypoxia-Inducible Factor-1α in Sensory Neurons.Journal of cardiovascular disease · 2013Article
- Evidence for a therapeutic effect of Braintone on ischemic brain damage.Neural regeneration research · 2013Article
- Adaptation to moderate hypoxia protects cortical neurons against ischemia-reperfusion injury and excitotoxicity independently of HIF-1α.Experimental neurology · 2011Article
- Selective inhibition of early--but not late--expressed HIF-1α is neuroprotective in rats after focal ischemic brain damage.Brain pathology (Zurich, Switzerland) · 2011Article
- Oxygen-regulated beta(2)-adrenergic receptor hydroxylation by EGLN3 and ubiquitylation by pVHL.Science signaling · 2009Article
- Prolyl hydroxylase inhibitors depend on extracellular glucose and hypoxia-inducible factor (HIF)-2alpha to inhibit cell death caused by nerve growth factor (NGF) deprivation: evidence that HIF-2alpha has a role in NGF-promoted survival of sympathetic neurons.Molecular pharmacology · 2009Article
- The von Hippel-Lindau protein sensitizes renal carcinoma cells to apoptotic stimuli through stabilization of BIM(EL).Oncogene · 2009Article
- VHL mutations linked to type 2C von Hippel-Lindau disease cause extensive structural perturbations in pVHL.The Journal of biological chemistry · 2009Article
- Mitochondrial Ca2+ overload underlies Abeta oligomers neurotoxicity providing an unexpected mechanism of neuroprotection by NSAIDs.PloS one · 2008Article
- Abnormal sympathoadrenal development and systemic hypotension in PHD3-/- mice.Molecular and cellular biology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Changes in O(2) tension can significantly impact cell survival, yet the mechanisms underlying these effects are not well understood. Here, we report that maintaining sympathetic neurons under low O(2) inhibits apoptosis caused by NGF deprivation. Low O(2) exposure blocked cytochrome c release after NGF withdrawal, in part by suppressing the up-regulation of BIM(EL). Forced BIM(EL) expression removed the block to cytochrome c release but did not prevent protection by low O(2). Exposing neurons to low O(2) also activated hypoxia-inducible factor (HIF) and expression of a stabilized form of HIF-1alpha (HIF-1alpha(PP-->AG)) inhibited cell death in normoxic, NGF-deprived cells. Targeted deletion of HIF-1alpha partially suppressed the protective effect of low O(2), whereas deletion of HIF-1alpha combined with forced BIM(EL) expression completely reversed the ability of low O(2) to inhibit cell death. These data suggest a new model for how O(2) tension can influence apoptotic events that underlie trophic factor deprivation-induced cell death.
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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.