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The Weakened Interaction Between HECTD4 and GluN2B in Ischemic Stroke Promotes Calcium Overload and Brain Injury Through a Mechanism Involving the Decrease of GluN2B and MALT1 Ubiquitination
This study explores the relationship between HECTD4, GluN2B, and MALT1, focusing on their role in brain injury in ischemic stroke. Rats were subjected to 2  h-ischemia followed by 24-h reperfusion to establish an ischemic stroke model. We observed the downregulation of HECTD4 and the upregulation of MALT1. Additionally, an increased GluN2B phosphorylation was concomitant with weakened interactions between HECTD4 and GluN2B, followed by decreased stria tal-enriched protein phosphatase (STEP61). Knockdown of HECTD4 exacerbated hypoxia- or NMDA-induced injury in nerve cells coincident with a decrease in GluN2B and MALT1 ubiq...
Source: Molecular Neurobiology - March 1, 2023 Category: Neurology Source Type: research

NAMPT as a Dedifferentiation-Inducer Gene: NAD+ as Core Axis for Glioma Cancer Stem-Like Cells Maintenance
Conclusion and Perspectives Gliomas are the most prevalent primary brain cancer in adults and include a broad category of tumors including astrocytoma, oligodendroglioma, and GBM. Regardless of tumor aggressiveness, malignancy, and infiltration, these glia-derived tumors rarely exceed a median survival time of 12–14 months. Driven by the infiltrative nature of these tumors, the clinical approach is difficult and relapses often occur with fatal consequences. These unsuccessful attempts to control glioma's fate have fostered research looking for more effective therapies. (GSCs) are a small subset of CD133&#...
Source: Frontiers in Oncology - May 2, 2019 Category: Cancer & Oncology Source Type: research

Cryptotanshinone Attenuates Oxygen-Glucose Deprivation/ Recovery-Induced Injury in an in vitro Model of Neurovascular Unit
Conclusions Despite the above limitations, we indicate that the protective mechanism of CTs against OGD/R damage might exert via inhibiting neuron apoptosis and attenuating BBB disruption. Furthermore, we also clarified that CTs inhibited neuronal apoptosis possibly by blocking the activation of MAPK signaling pathways, and CTs alleviating BBB disruption may associated with the regulation of TJPs and MMP-9 in our experiment. Accordingly, CTs will represent a novel and potent candidate for the treatment of CIRI in the future. Ethics Statement This study was carried out in accordance with the recommendations of China�...
Source: Frontiers in Neurology - April 17, 2019 Category: Neurology Source Type: research

The Effects of Intelectin-1 on Antioxidant and Angiogenesis in HUVECs Exposed to Oxygen Glucose Deprivation
Conclusion: These results suggest intelectin-1 promotes angiogenesis, inhibits oxidative stress and reduces apoptosis by stimulating the Akt-eNOS signaling pathway in response to ischemia in vitro. Introduction Stroke is a main reason of human neurological disability, ischemic stroke (IS) accounts for almost 80–90% of all strokes. IS occurs after a cerebral blood flow disruption, leading to cellular death and tissue damage by restricting glucose and oxygen supplies (1). Ischemic vascular diseases cause substantial vascular valve and vascular endothelial cell injuries, eventually damaging the surrounding tis...
Source: Frontiers in Neurology - April 15, 2019 Category: Neurology Source Type: research

Novel endogenous negative modulators of platelet function as potential anti-thrombotic targets.
Authors: Li YJ, Zhu HX, Zhang D, Li HC, Ma P, Huang LY Abstract Platelets are megakaryocyte-derived nuclear-free fragments that participate in cardiovascular diseases including acute myocardial infarction, ischemic stroke, hypertension, and atherosclerosis. At the endothelium damage site, platelets interact with sub-endothelial matrix proteins such as glycoprotein VI/Fc receptor γ-chain (GPVI/FcRγ), G protein-coupled receptor/phospholipase Cγ(β) (GPCR/PLCγ(β)), Rho/RhoK and integrin. The activation of these signaling pathways triggers intracellular calcium increase and causes platelet adhesion, aggregation, g...
Source: European Review for Medical and Pharmacological Sciences - July 27, 2017 Category: Drugs & Pharmacology Tags: Eur Rev Med Pharmacol Sci Source Type: research

Calcium/calmodulin ‐dependent protein kinase kinase β is neuroprotective in stroke in aged mice
This study demonstrates that CaMKK β is neuroprotective following stroke in aged mice. Inhibition of CaMKK β worsened stroke outcome by reducing expression of prosurvival factors, as well as the levels of proteins important for the integrity of blood–brain barrier, and increasing proinflammatory cytokines in the serum after stroke. Conversely, the overexpression of CaMKK β reduced infarcts and behavioral deficits in aged mice.
Source: European Journal of Neuroscience - August 16, 2016 Category: Neuroscience Authors: Lin Liu, Hui Yuan, Kyle Denton, Xue ‐jun Li, Louise McCullough, Jun Li Tags: Clinical and Translational Neuroscience Source Type: research

Calcium/Calmodulin ‐Dependent Protein Kinase Kinase β (CaMKK β) is Neuroprotective in Stroke in Aged Mice
This article is protected by copyright. All rights reserved.
Source: European Journal of Neuroscience - June 15, 2016 Category: Neuroscience Authors: Lin Liu, Hui Yuan, Kyle Denton, Xue ‐jun Li, Louise McCullough, Jun Li Tags: Research Report Source Type: research

Calcium/Calmodulin‐Dependent Protein Kinase Kinase β (CaMKK β) is Neuroprotective in Stroke in Aged Mice
This article is protected by copyright. All rights reserved.
Source: European Journal of Neuroscience - June 15, 2016 Category: Neuroscience Authors: Lin Liu, Hui Yuan, Kyle Denton, Xue‐jun Li, Louise McCullough, Jun Li Tags: Research Report Source Type: research

EP3, Prostaglandin E2 Receptor Subtype 3, Associated with Neuronal Apoptosis Following Intracerebral Hemorrhage.
Abstract EP3 is prostaglandin E2 receptor subtype 3 and mediates the activation of several signaling pathways, changing in cAMP levels, calcium mobilization, and activation of phospholipase C. Previous studies demonstrated a direct role for EP3 in various neurodegenerative disorders, such as stroke and Alzheimer disease. However, the distribution and function of EP3 in ICH diseases remain unknown. Here, we demonstrate that EP3 may be involved in neuronal apoptosis in the processes of intracerebral hemorrhage (ICH). From the results of Western blot and immunohistochemistry, we obtained a significant up-regulation o...
Source: Cellular and Molecular Neurobiology - December 30, 2015 Category: Cytology Authors: Ni H, Shen J, Song Y, Cao M, Liu X, Huang J, Zhang W, Xie L, Ning X, Ke K Tags: Cell Mol Neurobiol Source Type: research

Genetic deletion of calcium/calmodulin-dependent protein kinase kinase ß (CaMKK ß) or CaMK IV exacerbates stroke outcomes in ovariectomized (OVXed) female mice
Conclusions: Inhibition of CaMKK signaling exacerbated stroke outcome and increased BBB impairment, transcriptional inactivation and inflammatory responses in females after stroke. Therefore, CaMKK signaling may be a potential target for stroke treatment in both males and females.
Source: BMC Neuroscience - October 21, 2014 Category: Neuroscience Authors: Lin LiuLouise McCulloughJun Li Source Type: research

Summary: International Kidney Cancer Symposium
Conclusions:  Ideal ischemia time is 20-25 minutes or less improves short and long term renal function.  >25 minutes carried 5 year risk of new onset stage 4 CKD No differences on GFR for cold vs. warm ischemia times Preoperative GFR and the percent of kidney preserved was a better predictor of post op GFR.  No ischemia preserves renal function better than warm. Longer cold ischemia times were equivalent to shorter warm ischemia times. Quality and quantity of the remaining kidney is associated with ultimate renal function. Robotics in RCC Surgery Gennady Bratslavsky, MD The...
Source: Kidney Cancer Association - December 15, 2011 Category: Urology & Nephrology Source Type: news