ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Survivin Is a transcriptional target of STAT3 critical to estradiol neuroprotection in global ischemia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.Inflammopharmacology · 2025Article
- Gypenoside Pretreatment Alleviates the Cerebral Ischemia Injury via Inhibiting the Microglia-Mediated Neuroinflammation.Molecular neurobiology · 2024Article
- Piceatannol improved cerebral blood flow and attenuated JNK3 and mitochondrial apoptotic pathway in a global ischemic model to produce neuroprotection.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Immune regulation based on sex differences in ischemic stroke pathology.Frontiers in immunology · 2023Review
- Role of Endothelial STAT3 in Cerebrovascular Function and Protection from Ischemic Brain Injury.International journal of molecular sciences · 2022Article
- Over-expression of survivin could prevent the oxidative stress and toxicity of rotenone in SH-SY5Y cells.Iranian journal of basic medical sciences · 2022Article
- Article
- Sex-Associated Differences in Neurovascular Dysfunction During Ischemic Stroke.Frontiers in molecular neuroscience · 2022Review
- Association of BIRC5 Gene Polymorphism with the Collateral Circulation and Severity of Large Artery Atherosclerotic Stroke.International journal of clinical practice · 2022Article
- Renoprotective effects of estrogen on acute kidney injury: the role of SIRT1.International urology and nephrology · 2021Review
- The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina.International journal of molecular sciences · 2021Review
- Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Twist1 Plays an Anti-apoptotic Role in Mutant Huntingtin Expression Striatal Progenitor Cells.Molecular neurobiology · 2020Article
- STAT3 Contributes to Radioresistance in Cancer.Frontiers in oncology · 2020Review
- The Critical Period for Neuroprotection by Estrogen Replacement Therapy and the Potential Underlying Mechanisms.Current neuropharmacology · 2020Review
- Brusatol, a Nrf2 Inhibitor Targets STAT3 Signaling Cascade in Head and Neck Squamous Cell Carcinoma.Biomolecules · 2019Article
- A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis.Therapeutic hypothermia and temperature management · 2019Review
- Neuroprotective Effect of SCM-198 through Stabilizing Endothelial Cell Function.Oxidative medicine and cellular longevity · 2019Article
- Stimulation-dependent remodeling of the corticospinal tract requires reactivation of growth-promoting developmental signaling pathways.Experimental neurology · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transient global ischemia causes selective, delayed death of hippocampal CA1 pyramidal neurons in humans and animals. It is well established that estrogens ameliorate neuronal death in animal models of focal and global ischemia. However, the role of signal transducer and activator of transcription-3 (STAT3) and its target genes in estradiol neuroprotection in global ischemia remains unclear. Here we show that a single intracerebral injection of 17β-estradiol to ovariectomized female rats immediately after ischemia rescues CA1 neurons destined to die. Ischemia promotes activation of STAT3 signaling, association of STAT3 with the promoters of target genes, and STAT3-dependent mRNA and protein expression of prosurvival proteins in the selectively vulnerable CA1. In animals subjected to ischemia, acute postischemic estradiol further enhances activation and nuclear translocation of STAT3 and STAT3-dependent transcription of target genes. Importantly, we show that STAT3 is critical to estradiol neuroprotection, as evidenced by the ability of STAT3 inhibitor peptide and STAT3 shRNA delivered directly into the CA1 of living animals to abolish neuroprotection. In addition, we identify survivin, a member of the inhibitor-of-apoptosis family of proteins and known gene target of STAT3, as essential to estradiol neuroprotection, as evidenced by the ability of shRNA to survivin to reverse neuroprotection. These findings indicate that ischemia and estradiol act synergistically to promote activation of STAT3 and STAT3-dependent transcription of survivin in insulted CA1 neurons and identify STAT3 and survivin as potentially important therapeutic targets in an in vivo model of global ischemia.
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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.