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Glutamatergic CYLD deletion leads to aberrant excitatory activity in the basolateral amygdala: association with enhanced cued fear expression.
Neural Regen Res
November 2025
School of Life Sciences, South China Normal University, Guangzhou, Guangdong Province, China.
JOURNAL/nrgr/04.03/01300535-202511000-00029/figure1/v/2024-12-20T164640Z/r/image-tiff Neuronal activity, synaptic transmission, and molecular changes in the basolateral amygdala play critical roles in fear memory. Cylindromatosis (CYLD) is a deubiquitinase that negatively regulates the nuclear factor kappa-B pathway.
View Article and Find Full Text PDFAltered glia-neuron communication in Alzheimer's Disease affects WNT, p53, and NFkB Signaling determined by snRNA-seq.
Cell Commun Signal
June 2024
Department of Cell, Developmental and Integrative Biology, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL, United States of America.
Background: Alzheimer's disease is the most common cause of dementia and is characterized by amyloid-β plaques, tau neurofibrillary tangles, and neuronal loss. Although neuronal loss is a primary hallmark of Alzheimer's disease, it is known that non-neuronal cell populations are ultimately responsible for maintaining brain homeostasis and neuronal health through neuron-glia and glial cell crosstalk. Many signaling pathways have been proposed to be dysregulated in Alzheimer's disease, including WNT, TGFβ, p53, mTOR, NFkB, and Pi3k/Akt signaling.
View Article and Find Full Text PDFBotulinum toxin type A inhibits M1 macrophage polarization by deactivation of JAK2/STAT1 and IκB/NFκB pathway and contributes to scar alleviation in aseptic skin wound healing.
Biomed Pharmacother
May 2024
Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, Beijing, China. Electronic address:
Article Synopsis
- A study found that botulinum toxin type A (BTXA) can reduce scarring by affecting early skin repair processes and macrophage behavior in a rat model.
- BTXA was injected into skin wounds and showed significant reductions in scar size without slowing down healing, while improving tissue structure and inhibiting blood vessel growth.
- The treatment lowered the number of inflammatory M1 macrophages and reduced their activation pathways, helping to alleviate scar formation during the healing process.
Transient receptor potential vanilloid 1 interacts with Toll-like receptor 4 (TLR4)/cluster of differentiation 14 (CD14) signaling pathway in lipopolysaccharide-mediated inflammation in macrophages.
Exp Anim
July 2024
Graduate Institute and Department of Physiology, College of Medicine, National Taiwan University, 1, Sec. 1, Jen-Ai Road, Taipei 100233, Taiwan.
Transient receptor potential vanilloid 1 (TRPV1), a ligand-gated cation channel, is a receptor for vanilloids on sensory neurons and is also activated by capsaicin, heat, protons, arachidonic acid metabolites, and inflammatory mediators on neuronal or non-neuronal cells. However, the role of the TRPV1 receptor in pro-inflammatory cytokine secretion and its potential regulatory mechanisms in lipopolysaccharide (LPS)-induced inflammation has yet to be entirely understood. To investigate the role and regulatory mechanism of the TRPV1 receptor in regulating LPS-induced inflammatory responses, bone marrow-derived macrophages (BMDMs) harvested from wild-type (WT) and TRPV1 deficient (Trpv1) mice were used as the cell model.
View Article and Find Full Text PDFCellular forgetting, desensitisation, stress and ageing in signalling networks. When do cells refuse to learn more?
Cell Mol Life Sci
February 2024
Department of Molecular Biology, Semmelweis University, Budapest, Hungary.
Recent findings show that single, non-neuronal cells are also able to learn signalling responses developing cellular memory. In cellular learning nodes of signalling networks strengthen their interactions e.g.
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