In the present study, we aim to elucidate the role of caveolin-1 in modulating astroglial differentiation of neural progenitor cells (NPCs) and the potential mechanisms involved. We first investigated astroglial differentiation and Notch signaling by detecting the expressions of S100β, GFAP, NICD and hairy enhancer of split 1 (Hes1) in the brains of wild-type and caveolin-1 knockout mice. Caveolin-1 knockout mice revealed remarkably less astroglial differentiation and lower levels of NICD and Hes1 expressions than wild type mice. We then studied the potential roles of caveolin-1 in modulating NICD and Hes1 expressions and astroglial differentiation in isolated cultured NPCs by using caveolin-1 peptide and caveolin-1 RNA silencing. In the differentiating NPCs, caveolin-1 peptide markedly promoted astroglial formation and up-regulated the expressions of NICD and Hes1. In contrast, the knockdown of caveolin-1 inhibited astroglial differentiation of NPCs and the expressions of NICD and Hes1. Taken together, these results provide strong evidence that caveolin-1 can promote astroglial differentiation of NPCs through modulating Notch1/NICD and Hes1 expressions.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.bbrc.2011.03.050 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Aging and MPTP Sensitivity Depend on Molecular and Ultrastructural Signatures of Astroglia and Microglia in Mice Substantia Nigra.
Cell Mol Neurobiol
January 2025
Department of Neurophysiology, National Institute of Mental Health and Neurosciences, Hosur Road, Bengaluru, 560029, India.
Both astroglia and microglia show region-specific distribution in CNS and often maladapt to age-associated alterations within their niche. Studies on autopsied substantia nigra (SN) of Parkinson's disease (PD) patients and experimental models propose gliosis as a trigger for neuronal loss. Epidemiological studies propose an ethnic bias in PD prevalence, since Caucasians are more susceptible than non-whites.
View Article and Find Full Text PDFOctadecaneuropeptide promotes the migration of astrocyte via ODN metabotropic receptor and calcium signaling pathway.
Peptides
January 2025
University of Tunis El Manar, Faculty of Sciences of Tunis, LR18ES03 Laboratory of Neurophysiology, Cellular Physiopathology and Biomolecules Valorisation, Tunis 2092, Tunisia. Electronic address:
Migration is an essential characteristic of cells that occurs during many physiological and pathological processes. Astrocytes represent the most abundant cell type in the adult central nervous system (CNS), that play a crucial role in various functions such as guiding and supporting neuronal migration during development and maintaining brain homeostasis at adulthood. Astrocytes specifically synthesize and release endozepines, a family of regulatory peptides, including the octadecaneuropeptide (ODN).
View Article and Find Full Text PDFApolipoprotein E dysfunction in Alzheimer's disease: a study on miRNA regulation, glial markers, and amyloid pathology.
Front Aging Neurosci
December 2024
Department of Ophthalmology and Visual Sciences, Faculty of Medicine, Eye Care Centre, The University of British Columbia, Vancouver, BC, Canada.
Introduction: Apolipoprotein E (ApoE) plays a crucial role in lipid homeostasis, predominantly expressed in astrocytes and to a lesser extent in microglia within the central nervous system (CNS). While the allele is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), its precise role in AD pathogenesis remains elusive. -knockout (-ko) mice, mice expressing human , and human carriers exhibit similar deficits in lipid metabolism, cognitive and behavioral functions, and neurodegeneration.
View Article and Find Full Text PDFAgathisflavone Modulates Reactive Gliosis After Trauma and Increases the Neuroblast Population at the Subventricular Zone.
Nutrients
November 2024
Laboratory of Neurochemistry and Cellular Biology, Department of Biofunction, Health Sciences Institute, Federal University of Bahia, Salvador 40231-300, Brazil.
Background: Reactive astrogliosis and microgliosis are coordinated responses to CNS insults and are pathological hallmarks of traumatic brain injury (TBI). In these conditions, persistent reactive gliosis can impede tissue repopulation and limit neurogenesis. Thus, modulating this phenomenon has been increasingly recognized as potential therapeutic approach.
View Article and Find Full Text PDFGlial cell deficits are a key feature of schizophrenia: implications for neuronal circuit maintenance and histological differentiation from classical neurodegeneration.
Mol Psychiatry
December 2024
Department of Psychiatry, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany.
Dysfunctional glial cells play a pre-eminent role in schizophrenia pathophysiology. Post-mortem studies have provided evidence for significantly decreased glial cell numbers in different brain regions of individuals with schizophrenia. Reduced glial cell numbers are most pronounced in oligodendroglia, but reduced astrocyte cell densities have also been reported.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!