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β‐Catenin expression in human neural cell lines following exposure to cytokines and growth factors
Author(s) -
Satoh Junichi,
Kuroda Yasuo
Publication year - 2000
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1046/j.1440-1789.2000.00293.x
Subject(s) - biology , epidermal growth factor , basic fibroblast growth factor , endocrinology , medicine , growth factor , neurotrophic factors , cytokine , cell culture , cell growth , microbiology and biotechnology , transforming growth factor , wnt signaling pathway , signal transduction , cancer research , immunology , receptor , genetics
β‐Catenin acts as a key mediator of the Wnt/Wingless signaling pathway involved in cell proliferation, differentiation and survival. Recent studies have shown that an unstable interaction between β‐catenin and the mutant presenilin‐1 induces neuronal apoptosis, and that β‐catenin levels are decreased in the brains of patients with Alzheimer’s disease (AD). Since activated microglia and astrocytes play a role in the process of neuronal degeneration in AD, the cytokine/growth factor‐regulated expression of β‐catenin in human neural cell lines, including NTera2 teratocarcinoma‐derived differentiated neurons (NTera2‐N), IMR‐32 neuroblastoma, SKN‐SH neuroblastoma and U‐373MG astrocytoma, was studied quantitatively following exposure to epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), brain‐derived neurotrophic factor (BDNF), tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, interferon (IFN)‐γ, transforming growth factor (TGF)‐β1, dibutyryl cyclic adenosine 3′,5′‐cyclic monophosphate (cAMP) (dbcAMP) or phorbol 12‐myristate 13‐acetate (PMA). β‐Catenin mRNA expressed constitutively in all of these cell lines was unaffected by treatment with any factors examined. In contrast, β‐catenin protein levels were reduced markedly in NTera2‐N cells by exposure to dbcAMP, EGF or bFGF, and in U‐373MG cells by treatment with dbcAMP or PMA, but were unaffected in any cell lines by BDNF, TNF‐α, IL‐1β, IL‐6, IFN‐γ or TGF‐β1. These results indicate that β‐catenin is expressed constitutively in human neural cells and downregulated at a protein level by a set of growth factors in a cell type‐specific manner.