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Endocrine. 1995 Aug;3(8):549-56. doi: 10.1007/BF02953018.

TNF-α induces dyscohesion of epithelial cells. Association with disassembly of actin filaments.

Endocrine

S Tabibzadeh, Q F Kong, S Kapur, H Leffers, A Ridley, K Aktories, J E Celis

Affiliations

  1. Department of Pathology, University of South Florida Health Sciences Center and Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, Florida, USA.

PMID: 21153131 DOI: 10.1007/BF02953018

Abstract

TNF-α induced, in a time and dose-dependent fashion, cell-cell dissociation (dyscohesion) of endometrial epithelial cells. Within the time frame that dyscohesion was induced, TNF-α, in a dose-dependent fashion, reduced filamentous (F) actin and resulted in the loss of F-actin from the intercellular boundaries. Loss of F-actin mediated by TNF-α was not due to a reduction in the overall amount of actin or its β-isoform. Two proteins, Rho and Rho guanine nucleotide dissociation inhibitor (Rho-GDI), have been implicated in the regulation of organization of actin cytoskeleton. The reduced level of F-actin was not associated with altered expression of Rho protein, however, it was associated with an increase in the amount of Rho available for ribosylationin vitro by the C3 exoenzyme of Clostridium botulinum. The amount of Rho-GDI protein did not change after treatment with TNF-α suggesting that elevated expression of this protein is not responsible for the disassembly of actin filaments. These findings show that TNF-α induces dyscohesion. Dyscohesion induced by this cytokine is associated with perturbation of the actin cytoskeleton which may be due to the regulatory role of TNF-α on Rho.

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