Critical role of EphA4 in early brain injury after subarachnoid hemorrhage in rat.

Critical role of EphA4 in early brain injury after subarachnoid hemorrhage in rat. Exp Neurol. 2017 Jul 08;: Authors: Fan R, Enkhjargal B, Camara R, Yan F, Gong L, ShengtaoYao, Tang J, Chen Y, Zhang JH Abstract Early brain injury (EBI) is reported as a primary cause of mortality in subarachnoid hemorrhage (SAH) patients. Eph receptor A4 (EphA4) has been associated with blood-brain barrier integrity and pro-apoptosis. We aimed to investigate a role of EphA4 in EBI after SAH. One hundred and seventy-nine male adult Sprague-Dawley rats were randomly divided into sham versus endovascular perforation model of SAH groups. SAH grade, neurological score, Evans blue dye extravasation, brain water content, mortality, Fluoro-Jade staining, immunofluorescence staining, and western blot experiments were performed after SAH. Small interfering RNA (siRNA) for EphA4, recombinant Ephexin-1 (rEphx-1), and Fasudil, a potent ROCK2 inhibitor, were used for intervention to study a role of EphA4 on EBI after SAH. The expression of EphA4, Ephexin-1, RhoA, and ROCK2 significantly increased after SAH. Knockdown of EphA4 using EphA4 siRNA injection intracerebroventricularly (i.c.v) reduced Evans blue extravasation, decreased brain water content, and alleviated neurobehavioral dysfunction after SAH. Additionally, the expression of Ephexin-1, RhoA, ROCK2 and cleaved caspase-3 were decreased. Tight junction proteins increased, and apoptotic neuron death decreased. The effects of EphA...
Source: Experimental Neurology - Category: Neurology Authors: Tags: Exp Neurol Source Type: research

Related Links:

Authors: Chen H, Dang Y, Liu X, Ren J, Wang H Abstract Brain-derived neurotrophic factor (BDNF) is a growth factor crucial for neuronal survival, while its role in subarachnoid hemorrhage (SAH)-induced neuronal apoptosis remains unclear. The aim of the present study was to investigate whether administering exogenous BDNF can protect against neuronal apoptosis and neurological deficits following SAH in a rat model. The BDNF level was found to be significantly decreased in the basal cortex at 6, 12, 24, 48 and 72 h following SAH. Exogenous BDNF significantly decreased the expression of Bax and reduced activation of c...
Source: Experimental and Therapeutic Medicine - Category: General Medicine Tags: Exp Ther Med Source Type: research
In this study, we investigated the dynamics of microglial reaction in an endovascular perforated SAH model. By using the Cx3cr1GFP/GFP Ccr2RFP/RFP transgenic mice, we found that the reactive immune cells were largely from resident microglia pool rather than infiltrating macrophages. Immunostaining and real-time PCR were employed to analyze the temporal microglial polarization and the resulting inflammatory responses. Our results showed that microglia accumulated immediately after SAH with a centrifugal spreading through the Cortex Adjacent to the Perforated Site (CAPS) to the remote motor cortex. Microglia polarized dynami...
Source: Translational Stroke Research - Category: Neurology Source Type: research
ConclusionsSerum soluble LOX-1 appears to have the potential to become a promising prognostic predictor after human aneurysmal SAH.
Source: Clinica Chimica Acta - Category: Laboratory Medicine Source Type: research
CONCLUSIONS: Serum soluble LOX-1 appears to have the potential to become a promising prognostic predictor after human aneurysmal SAH. PMID: 31626762 [PubMed - as supplied by publisher]
Source: International Journal of Clinical Chemistry - Category: Chemistry Authors: Tags: Clin Chim Acta Source Type: research
In this study, we show that glycine can reduce brain edema and protect neurons in SAH via a novel pathway. Following a hemorrhagic episode, there is evidence of downregulation of S473 phosphorylation of AKT (p-AKT), and this can be reversed with glycine treatment. We also found that administration of glycine can reduce neuronal cell death in SAH by activating the AKT pathway. Glycine was shown to upregulate miRNA-26b, which led to PTEN downregulation followed by AKT activation, resulting in inhibition of neuronal death. Inhibition of miRNA-26b, PTEN or AKT activation suppressed the neuroprotective effects of glycine. Glyci...
Source: Neurochemical Research - Category: Neuroscience Authors: Tags: Neurochem Res Source Type: research
Conclusion: The ipsilateral ONP is a common sign found in posterior communicating artery aneurysms; however, such aneurysm can have different presentations due to the elevation of intracranial pressure, and, in rarer cases, the ONP cannot be operated as a localizing sign. PMID: 31583174 [PubMed]
Source: Surgical Neurology International - Category: Neurosurgery Tags: Surg Neurol Int Source Type: research
Background: Our previous study showed that propofol, one of the widely used anesthetic agents, can attenuate subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) via inhibiting inflammatory and oxidative reaction. However, it is perplexing whether propofol attenuates inflammatory and oxidative reaction through modulating PI3K/Akt pathway. The present study investigated whether PI3K/Akt pathway is involved in propofol's anti-inflammation, antioxidation, and neuroprotection against SAH-induced EBI.
Source: Journal of Stroke and Cerebrovascular Diseases - Category: Neurology Authors: Source Type: research
ConclusionSimple clinical features could help distinguish cSAH-associated TFNE from suspected TIA, with relevance for investigation and management, including the use of antithrombotic drugs.
Source: Journal of Neurology - Category: Neurology Source Type: research
Discussion: Results of the trial could provide insight into influence of lidocaine on local and systemic inflammatory response in cerebrovascular surgery, and might improve future anesthesia practice and treatment outcome. Trial is registered at NCT03823482.
Source: Medicine - Category: Internal Medicine Tags: Research Article: Study Protocol Clinical Trial Source Type: research
Conclusions: The peak time of PTH occurrence was noted during 0–3rd month post brain injury. Traumatic SAH patients had an approximate 3-fold risk of developing PTH, comparing to TBI patients without traumatic SAH.
Source: Medicine - Category: Internal Medicine Tags: Research Article: Observational Study Source Type: research
More News: Brain | Hemorrhagic Stroke | Neurology | Study | Subarachnoid Hemorrhage