• Filter By:
• Specialty
• Source
• Condition
• Cancer
• Infectious Disease
• Drug
• Training
• Management
• Procedure
• Therapy
• Vaccine
• Nutrition
• Country

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

Retinoic Acid Prevents the Neuronal Damage Through the Regulation of Parvalbumin in an Ischemic Stroke Model
In conclusion, retinoic acid contributes to the preservation of neurons from ischemic stroke by controlling parvalbumin expression and apoptosis-related proteins.PMID:36245066 | DOI:10.1007/s11064-022-03769-9
Source: Neurochemical Research - October 16, 2022 Category: Neuroscience Authors: Ju-Bin Kang Dong-Ju Park Phil-Ok Koh Source Type: research

Hypothermia Promotes Mitochondrial Elongation In Cardiac Cells Via Inhibition Of Drp1
In conclusion hypothermia promoted elongation of cardiac mitochondria via reduced pDrp1S616 abundance which was also associated with suppression of cellular oxygen consumption. Silencing of TRPV1 in H9c2 cardiomyocytes reproduced the morphological and respirometric phenotype of hypothermia. This report demonstrates a novel mechanism of cold-induced inhibition of mitochondrial fission.PMID:34331901 | DOI:10.1016/j.cryobiol.2021.07.013
Source: Cryobiology - July 31, 2021 Category: Biology Authors: David Taylor Juliana Germano Yang Song Hanane Hadj-Moussa Stefanie Marek-Iannucci Raeesa Dhanji Jon Sin Lawrence S C Czer Kenneth B Storey Roberta A Gottlieb Source Type: research

Inhibition of Calcium/Calmodulin-Dependent Protein Kinase II α Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase.
Inhibition of Calcium/Calmodulin-Dependent Protein Kinase IIα Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase. Neurochem Res. 2019 Mar 27;: Authors: Wei Y, Wang R, Teng J Abstract Ischemic stroke is a leading cause of mortality and morbidity worldwide, and oxidative stress plays a significant role in the ischemia stage and reperfusion stage. Previous studies have indicated that both calcium/calmodulin-dependent protein kinase II (CaMKII) and glucose 6-phosphate dehydrogenase (G6PD) are involved in the oxidative stress. Thus, the aim of this st...
Source: Neurochemical Research - March 26, 2019 Category: Neuroscience Authors: Wei Y, Wang R, Teng J Tags: Neurochem Res Source Type: research

Mfn2-Mediated Preservation of Mitochondrial Function Contributes to the Protective Effects of BHAPI in Response to Ischemia
This study investigated the protective effects of N ′-(1-(2-((4-(4,4,5,5-tetramethyl-1,2,3-dioxoborolan-2-yl)benzyl)oxy)phenyl)ethylidene (BHAPI) on an in vitro ischemia model mimicked by oxygen and glucose deprivation (OGD) in neuronal HT22 cells. The results showed that BHAPI significantly increased cell viability and decreased lactate dehydrogen ase (LDH) release after OGD. BHAPI treatment also reduced apoptosis, as measured by flow cytometry, and suppressed caspase-3 activation. These protective effects were accompanied by preserved mitochondrial membrane potential (MMP), reduced mitochondrial swelling, promoted mito...
Source: Journal of Molecular Neuroscience - September 26, 2017 Category: Neuroscience Source Type: research