
Neuroscience Letters, Journal Year: 2023, Volume and Issue: 809, P. 137305 - 137305
Published: May 18, 2023
Language: Английский
Neuroscience Letters, Journal Year: 2023, Volume and Issue: 809, P. 137305 - 137305
Published: May 18, 2023
Language: Английский
Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 253, P. 155085 - 155085
Published: Jan. 1, 2024
Language: Английский
Citations
2Molecular Neurobiology, Journal Year: 2024, Volume and Issue: unknown
Published: April 1, 2024
Language: Английский
Citations
2Cells, Journal Year: 2022, Volume and Issue: 11(1), P. 158 - 158
Published: Jan. 4, 2022
Williams syndrome (WS) is a multisystem neurodevelopmental disorder caused by de novo hemizygous deletion of ~26 genes from chromosome 7q11.23, among them the general transcription factor II-I (GTF2I). By studying novel murine model for hypersociability phenotype associated with WS, we previously revealed surprising aberrations in myelination and cell differentiation properties cortices mutant mice compared to controls. These had selective Gtf2i excitatory neurons forebrain. Here, applied diffusion magnetic resonance imaging fiber tracking, which showed reduction number streamlines limbic outputs such as fimbria/fornix fibers stria terminalis, well corpus callosum these Furthermore, utilized next-generation sequencing (NGS) analysis cortical small RNAs' expression (RNA-Seq) levels identify altered microRNAs (miRNAs), including two miR-34 cluster, known be involved prominent processes developing nervous system. Luciferase reporter assay confirmed direct binding miR-34c-5p 3'UTR PTPRU-a gene neural development that was elevated relative Moreover, found an age-dependent variation doublecortin (Dcx)-a verified target. Thus, demonstrate substantial effect single can exert on miRNA regulation brain structure, advance our understanding and, hopefully, treatment WS.
Language: Английский
Citations
11Journal of Biochemical and Molecular Toxicology, Journal Year: 2021, Volume and Issue: 35(6), P. 1 - 11
Published: March 24, 2021
Abstract Previous studies have suggested that microRNA‐186 (miR‐186) can be induced under hypoxic conditions, and is associated with apoptosis. This study was undertaken to explore the exact role of this microRNA (miRNA) in apoptotic death neurons during cerebral ischemic/reperfusion (I/R) injury. To model ischemia/reperfusion injuries, we utilized a transient middle artery occlusion approach rats, as well oxygen‐glucose deprivation/reoxygenation (OGD/R) Neuro2a cells. We found both vitro vivo models I/R levels miR‐186 were markedly decreased. When overexpressed miR‐186, reduction neuroblastoma cells OGD/R system, whereas opposite true when miRNA instead inhibited. further directly target hypoxia‐inducible factor 1α (HIF‐1α) by interacting 3′‐untranslated region mRNA. knocked down HIF‐1α, partially overcame response injury downregulation. Our findings indicate able reduce ischemic at least part through downregulating suggesting miR‐186/HIF‐1α axis potential therapeutic for treatment stroke.
Language: Английский
Citations
13Neuroscience Letters, Journal Year: 2023, Volume and Issue: 809, P. 137305 - 137305
Published: May 18, 2023
Language: Английский
Citations
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