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Transforming growth factors-β protect primary rat hippocampal neuronal cultures from degeneration induced by β-amyloid peptide

Authors
Journal
Brain Research
0006-8993
Publisher
Elsevier
Publication Date
Volume
732
Identifiers
DOI: 10.1016/0006-8993(96)00458-1
Keywords
  • Transforming Growth Factor-β
  • β-Amyloid Peptide
  • Alzheimer'S Disease
  • Neuroprotection
  • Primary Hippocampal
  • Neuron
  • Neuroblastoma Cell Line
Disciplines
  • Medicine

Abstract

Abstract Treatment of primary rat embryo hippocampal neuronal cultures with 10 −5 M β-amyloid peptide fragment 25–35 (AβP) for 24 h resulted in a 60% decrese in cell viability as determined by MTT incorporation. When these cells were treated with 0.1–10 ng/ml of either transforming growth factor-β (TGF-β) 1, 2 or 3 for 24 h before exposure to AβP, there was a 2.9-, 1.9-, and 3.2-fold increase in cell survival, respectively, compared to cells treated with AβP alone. The viability of cells treated with AβP and 0.1–10 ng/ml TGF-β was comparable to that of cells not treated with AβP. The protective effects were less pronounced at lower TGF-β concentrations. The protective effects of pretreatment with TGF-β were less striking in mouse CCL-N-2a and human SK-N-SH neuroblastoma cell lines. When all cells were treated with TGF-β for 24 h following a 24 h exposure to AβP, there was a trend toward increased cell viability which was less significant than pretreatment with TGFs-β. An isoform-specific TGF-β SELISA showed that primary hippocampal neuronal cultures and the neuroblastoma cell lines secrete all 3 TGF-β isoforms. Based on our results, we propose that the increased expression of TGF-β observed in brains of patients with Alzheimer's disease may offer some degree of neuroprotection.

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