ArticleNeuroscience2015
Pharmacological induction of the 70-kDa heat shock protein protects against brain injury.
Article in Neuroscience, 2015. 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, 40 citations in OpenAlex.
- Traumatic brain injury induces cell-type-specific remodelling of the proteostasis network.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Experimental traumatic brain injury increases epichaperome formation.Neurobiology of disease · 2023Article
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
- Targeting HSP47 and HSP70: promising therapeutic approaches in liver fibrosis management.Journal of translational medicine · 2022Review
- Synergistic effects of brain injury and aging: common mechanisms of proteostatic dysfunction.Trends in neurosciences · 2021Review
- Exposure to 2.45 GHz Radiation Triggers Changes in HSP-70, Glucocorticoid Receptors and GFAP Biomarkers in Rat Brain.International journal of molecular sciences · 2021Article
- Intrinsic Aerobic Capacity Affects Hippocampal pAkt and HSP72 Response to an Acute High Fat Diet and Heat Treatment in Rats.Journal of Alzheimer's disease reports · 2021Article
- Heat Shock Protein 70 (HSP70) Induction: Chaperonotherapy for Neuroprotection after Brain Injury.Cells · 2020Review
- Article
- Dynamic neural and glial responses of a head-specific model for traumatic brain injury inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Inhibition of Hsp90 in the spinal cord enhances the antinociceptive effects of morphine by activating an ERK-RSK pathway.Science signaling · 2020Article
- Pyrrolylquinoxaline-2-One Derivative as a Potent Therapeutic Factor for Brain Trauma Rehabilitation.Pharmaceutics · 2020Article
- Heat shock protein signaling in brain ischemia and injury.Neuroscience letters · 2020Review
- Inflammation in Traumatic Brain Injury.Journal of Alzheimer's disease : JAD · 2020Review
- Inhibiting Heat Shock Protein 90 Protects Nucleus Pulposus-Derived Stem/Progenitor Cells From Compression-Induced Necroptosis and Apoptosis.Frontiers in cell and developmental biology · 2020Article
- Microglial Calcium Release-Activated Calcium Channel Inhibition Improves Outcome from Experimental Traumatic Brain Injury and Microglia-Induced Neuronal Death.Journal of neurotrauma · 2019Article
- Heat-Shock Proteins in Neuroinflammation.Frontiers in pharmacology · 2019Review
- The 70-kDa heat shock protein (Hsp70) as a therapeutic target for stroke.Expert opinion on therapeutic targets · 2018Review
- Review
- Heat-shock protein 90 (Hsp90) promotes opioid-induced anti-nociception by an ERK mitogen-activated protein kinase (MAPK) mechanism in mouse brain.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The 70-kDa heat shock protein (HSP70) is known to protect the brain from injury through multiple mechanisms. We investigated the effect of pharmacological HSP70 induction in experimental traumatic brain injury (TBI). 3-month-old male C57/B6 mice were given 17-N-allylamino-17-demethoxygeldanamycin (17-AAG) intraperitoneally (IP, 2 mg/kg) or intracerebroventricularly (ICV, 1 μg/kg) to determine whether HSP70 could be induced in the brain. Mice were subjected to TBI via cortical controlled impact, and were treated with 17-AAG (or vehicle) IP according to one of two treatment regimens: (1) 2 mg/kg at the time of injury, (2) a total of three doses (4 mg/kg) at 2 and 1d prior to TBI and again at the time of injury. Brains were assessed for HSP70 induction, hemorrhage volume at 3 d, and lesion size at 14 d post-injury. Immunohistochemistry showed that both IP and ICV administration of 17-AAG increased HSP70 expression primarily in microglia and in a few neurons by 24 h but not in astrocytes. 17-AAG induced HSP70 in injured brain tissue as early as 6 h, peaking at 48 h and largely subsiding by 72 h after IP injection. Both treatment groups showed decreased hemorrhage volume relative to untreated mice as well as improved neurobehavioral outcomes. These observations indicate that pharmacologic HSP70 induction may prove to be a promising treatment for TBI.
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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.