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We studied the involvement of two members of the CCAAT/enhancer binding proteins (C/EBPs) family of transcription factors, C/EBPalpha and C/EBPbeta, in glial activation induced by different stimuli in rat cerebellar neuronal-glial cultures. Glial activation was induced by two types of neuronal death--excitotoxic and apoptotic. We had previously reported that these two induction mechanisms resulted in different patterns of glial activation (K. Pérez-Capote, J. Serratosa, C. Solà, Excitotoxic and apoptotic neuronal death induce different patterns of glial activation in vitro, J. Neurochem. 94 (2005) 226-237), only the former involving an inflammatory response. Glial activation was also induced by lipopolysaccharide (LPS) from E. coli, an inflammatory agent with a known direct effect on glial cells. Using immunocytochemical techniques, here we examined whether changes in C/EBPalpha and C/EBPbeta expression are selectively associated with a determinate pattern of glial activation. Excitotoxic neuronal death increased glial C/EBPbeta expression in the absence of alterations in C/EBPalpha expression, while no effect was observed following neuronal apoptosis. LPS treatment decreased C/EBPalpha and increased C/EBPbeta expression in glial cells. These results implicate C/EBPs in glial activation, although these two factors appear to have different roles. C/EBPalpha expression decreases only in response to LPS, while C/EBPbeta expression is increased by both LPS and excitotoxic neuronal death, although not by neuronal apoptosis. These results show that C/EBPbeta plays an active role in glial activation, but only when this involves an inflammatory reaction, suggesting a role for C/EBPbeta in neuroinflammation.
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http://dx.doi.org/10.1016/j.neulet.2006.09.078 | DOI Listing |
J Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFBackground: Devoid of a lymphatic system, the central nervous system (CNS) relies primarily on innate immunity for protection. While these immune responses help to fight pathogens, they can also cause irreversible damage because of the CNS's limited regenerative capacity. Therefore, it is crucial to understand which CNS cells contribute to pathogen clearance but in doing so potentially damage surrounding tissue.
View Article and Find Full Text PDFNeuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFJ Anat
September 2025
Department of Anatomy and Cell Biology, Hyogo Medical University School of Medicine, Nishinomiya, Hyogo, Japan.
The white matter of the spinal cord is essential for sensory and motor signaling, and its proper development is crucial for establishing functional neuronal circuits. However, the mechanisms underlying white matter formation remain incompletely understood. We hypothesized that the extracellular matrix, particularly laminins, plays a key role in this process.
View Article and Find Full Text PDFStem Cell Reports
September 2025
Neural Stem Cells and Neuroimaging Group, Department of Neurobiology, Hellenic Pasteur Institute, 11521 Athens, Greece. Electronic address:
In the adult brain, neural stem cells (NSCs) constitutively generate new neurons in specific neurogenic domains. Recent research has unveiled reactive neurogenesis, whereby brain injury triggers NSC activation, enhancing their differentiation potential and guiding progeny to injured areas. Our study provides evidence of alternative migration pathways for newborn neurons in the mouse subcortical forebrain, revealed by administration of a chemotherapeutic agent.
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