The spinal cord and hippocampal primary cultures were incubated with three neurotoxins (separately) known to impair the main components of the cytoplasmic cytoskeleton: 1) colchicine blocking the repolymerization of microtubules, 2) cytochalasin preventing elongation of actin filaments, and 3) beta, beta'-iminodipropionitrile (IDPN), causing disorganisation of neurofilaments. The distribution of surface membrane molecules on the surface of the neurons was evaluated in the ultrastructural study after treatment with the neurotoxins on the 5th, 12th, and 15th days in vitro (DIV). On the 12 DIV, the density of immunogold labelled neural cell adhesion molecules (NCAM) on IDPN-treated hippocampal neurons increased 1.45 times comparing to the controls. On the 5 DIV, the density of WGA (wheat germ agglutinin)-binding membrane glycoproteins increased 2.09 times on colchicine-treated neurons, and 3.98 times on cytochalasin-treated ones, whereas on the 12 DIV, the increase was 3.28 and 2.72 times, respectively, as compared to the control cultures of the same age. These data provide insights into the mechanisms of neurodegenerative changes in the nerve cells and into the relationship between the cytoskeletal elements and the surface molecules on the neuronal plasmatic membrane.
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Redox Biol
January 2025
Redox Biology Group, Danish Cancer Institute, 2100, Copenhagen, Denmark. Electronic address:
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Instituto de Biociências, Universidade Estadual Paulista (UNESP), Botucatu, Brazil.
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Division of Biomedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, 300 Prince Philip Drive, St. Johns, NL A1B 3V6, Canada.
Cell immortalization corresponds to a biologically relevant clinical feature that allows cells to acquire a high proliferative potential during carcinogenesis. In multiple cancer types, Protein Kinase D3 (PKD3) has often been reported as a dysregulated oncogenic kinase that promotes cell proliferation. Using mouse embryonic fibroblasts (MEFs), in a spontaneous immortalization model, PKD3 has been demonstrated as a critical regulator of cell proliferation after immortalization.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Frontier Health Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, 7-2-10 Higashiogu, Arakawa-Ku, 116-8551, Tokyo, Japan. Electronic address:
Actin linked regulatory mechanisms are known to contribute contraction/relaxation in smooth muscle. In order to clarify whether modulation of polymerization/depolymerization of actin filaments affects relaxation process, we examined the effects of cytochalasin D on relaxation process by Ca removal after Ca-induced contraction of β-escin skinned (cell membrane permeabilized) taenia cecum and carotid artery preparations from guinea pigs. Cytochalasin D, an inhibitor of actin polymerization, significantly suppressed the force during relaxation both in skinned taenia cecum and carotid artery.
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