ArticleNeurobiology of disease2015
Development-dependent regulation of molecular chaperones after hypoxia-ischemia.
Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Involvement of heat shock proteins HSP70 in the mechanisms of endogenous neuroprotection: the prospect of using HSP70 modulators.Frontiers in cellular neuroscience · 2023Pooled it
- Cannabidiol effectively prevents oxidative stress and stabilizes hypoxia-inducible factor-1 alpha (HIF-1α) in an animal model of global hypoxia.Scientific reports · 2024Article
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Chaperones vs. oxidative stress in the pathobiology of ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- The Role of Mitochondrial and Endoplasmic Reticulum Reactive Oxygen Species Production in Models of Perinatal Brain Injury.Antioxidants & redox signaling · 2019Article
- Characterization of Gene Expression in the Rat Brainstem After Neonatal Hypoxic-Ischemic Injury and Antioxidant Treatment.Molecular neurobiology · 2017Article
- The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia.Journal of neuroinflammation · 2017Article
- Evidence of cellular stress and caspase-3 resulting from a combined two-frequency signal in the cerebrum and cerebellum of sprague-dawley rats.Oncotarget · 2016Article
- Endoplasmic reticulum pathology and stress response in neurons precede programmed necrosis after neonatal hypoxia-ischemia.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2016Article
- Targeting Glial Mitochondrial Function for Protection from Cerebral Ischemia: Relevance, Mechanisms, and the Role of MicroRNAs.Oxidative medicine and cellular longevity · 2016Review
- Hypothermia and Rewarming Activate a Macroglial Unfolded Protein Response Independent of Hypoxic-Ischemic Brain Injury in Neonatal Piglets.Developmental neuroscience · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular stress response after hypoxia-Ischemia (HI) may be substantially different between immature and mature brains. To study this phenomenon, postnatal day 7 (P7) and P26 rats were subjected to HI followed by different periods of recovery. Nuclear accumulation of heat-shock transcription factor-1 (HSF1) and expression of molecular chaperone proteins and mRNAs were analyzed by in situ hybridization, Western blotting and confocal microscopy. Nuclear accumulation of HSF1 protein and induction of hsp70 mRNA occurred dramatically in P26 neurons, but minimally in P7 neurons and moderately in microglial cells after HI. Consistently, the level of HSF1 was significantly higher in P26 brain samples, compared with that in P7 brain. Translation of hsp70 mRNA into proteins in P26 mature neurons was seen at 4h and peaked at 24h, when some neurons had already died after HI. Induction of ER glucose-regulated protein-78 (grp78) and mitochondrial hsp60 mRNAs and proteins was moderate and occurred also only in P26 mature brain after HI. These results suggest that the cellular stress response after HI is development-dependent, being pronounced in mature but virtually negligible in neonatal neurons. Therefore, the effectiveness of therapeutic strategies targeting the stress pathway against HI may be significantly different between immature and mature brains. The delayed induction of molecular chaperones in mature brain may be somewhat late for protecting HI neurons from acute HI injury.
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