Project description:To investigate the endothelial-mesenchymal transition in cerebral arteriovenous malformation. We performed gene expression profiling analysis using the data obtained from RNA-seq of CD31+CD45- brain cells in Cdh5cre;Mgpflox/flox mice with or without tamoxifen induction.
Project description:Brain arteriovenous malformation (BAVM) is a high-flow vascular shunt that predisposes to intracranial hemorrhage and represents a leading cause of stroke in young adults. Somatic mutations in KRAS or BRAF drive endothelial dysfunction and lesion formation, yet the contribution of non-endothelial cells within the neuro-glial-vascular unit remains incompletely understood.
Project description:This study presents a quantitative proteomic analysis of human brain arteriovenous malformation (AVM) tissues with different rupture status. Surgically resected AVM specimens from ruptured and unruptured lesions were subjected to protein extraction, enzymatic digestion, and liquid chromatography–tandem mass spectrometry (LC-MS/MS) analysis. The dataset aims to characterize proteomic alterations associated with hemorrhagic presentation and to identify molecular pathways potentially involved in vascular instability. Raw mass spectrometry data and processed identification results are provided to facilitate data reuse and integrative multi-omics analyses.
Project description:Cerebral arteriovenous malformations (AVMs) are the most common vascular malformations worldwide and the leading cause of hemorrhagic strokes that result in crippling neurological deficits. Here, using newly generated mouse model, we discovered that genome-wide ocuppancy of H4K8ac and H3K27me3 decreased in mouse cerebral AVMs.
Project description:Mitochondrial transfer from astrocytes to endothelial cells reinforces redox homeostasis and barrier integrity in brain arteriovenous malformation