ArticleJournal of molecular neuroscience : MN2019
Inhibition of EPAC2 Attenuates Intracerebral Hemorrhage-Induced Secondary Brain Injury via the p38/BIM/Caspase-3 Pathway.
Article in Journal of molecular neuroscience : MN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
- Review
- Inhibition of EPAC1 Prevents Neuronal Death Mediated by Diesel Exhaust Particles in Ferroptotic Cell Death Conditions.Antioxidants (Basel, Switzerland) · 2026Article
- Selective Epac2 antagonist attenuates cerebral infarction induced by secondary brain injury in rats.Experimental and therapeutic medicine · 2025Article
- MIC19 Exerts Neuroprotective Role via Maintaining the Mitochondrial Structure in a Rat Model of Intracerebral Hemorrhage.International journal of molecular sciences · 2023Article
- LncRNA-PEAK1 promotes neuronal apoptosis after intracerebral hemorrhage by miR-466i-5p/caspase 8 axis.Heliyon · 2023Article
- Sam50 exerts neuroprotection by maintaining the mitochondrial structure during experimental cerebral ischemia/reperfusion injury in rats.CNS neuroscience & therapeutics · 2022Article
- Pharmacological Inhibition of Epac1 Averts Ferroptosis Cell Death by Preserving Mitochondrial Integrity.Antioxidants (Basel, Switzerland) · 2022Article
- Epac: A Promising Therapeutic Target for Vascular Diseases: A Review.Frontiers in pharmacology · 2022Review
- Effects and Mechanism of Oxymatrine Combined with Compound Yinchen Granules on the Apoptosis of Hepatocytes through the Akt/FoxO3a/Bim Pathway.BioMed research international · 2022Article
- Loss of MIC60 Aggravates Neuronal Death by Inducing Mitochondrial Dysfunction in a Rat Model of Intracerebral Hemorrhage.Molecular neurobiology · 2021Article
- miR‑3613‑3p/MAP3K2/p38/caspase‑3 pathway regulates the heat‑stress‑induced apoptosis of endothelial cells.Molecular medicine reports · 2021Article
- Epac: new emerging cAMP-binding protein.BMB reports · 2021Review
- The therapeutic potential of targeting exchange protein directly activated by cyclic adenosine 3',5'-monophosphate (Epac) for central nervous system trauma.Neural regeneration research · 2021Review
- Selective small-molecule EPAC activators.Biochemical Society transactions · 2019Review
- Epac2 Elevation Reverses Inhibition by Chondroitin Sulfate ProteoglycansThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Exchange proteins directly activated by cAMP (EPACs) are critical cAMP-dependent signaling pathway intermediaries that have been implicated in the pathogenesis of several human diseases, particularly neurological disorders. However, their pathogenic role in secondary brain injury (SBI) induced by intracranial hemorrhage (ICH) is unknown. The aim of this study was to examine the effects of EPAC2 on ICH-induced SBI and its underlying mechanisms. An in vivo ICH model was established in Sprague-Dawley rats by autologous blood injection. In addition, rat primary cortical neuronal cultures were exposed to oxyhemoglobin to simulate ICH in vitro. The function of EPAC2 in SBI induced by ICH was studied using the EPAC2-specific inhibitor ESI-05. In this study, we found that EPAC2 protein expression was significantly increased in the ICH models in vitro and in vivo. Furthermore, EPAC2 activation was inhibited by ESI-05 under ICH conditions. Inhibition of EPAC2 decreased the apoptosis rate of nerve cells in the cortex accompanied by a corresponding decrease in the protein expression of phosphorylated p38, Bcl-2-like protein 11 (BIM), and caspase-3. In summary, this study showed that inhibition of EPAC2 activation by ESI-05 suppressed SBI induced by ICH via the p38/BIM/caspase-3 signaling pathway.
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