Beta Amyloid Suppresses the Expression of the Vitamin D Receptor Gene and Induces the Expression of the Vitamin D Catabolic Enzyme Gene in Hippocampal Neurons

Dursun E., Gezen-Ak D., Yilmazer S.

DEMENTIA AND GERIATRIC COGNITIVE DISORDERS, cilt.36, ss.76-86, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 36
  • Basım Tarihi: 2013
  • Doi Numarası: 10.1159/000350319
  • Dergi Adı: DEMENTIA AND GERIATRIC COGNITIVE DISORDERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.76-86
  • İstanbul Üniversitesi Adresli: Evet

Özet

Background/Aims: The beta amyloid aggregations present in Alzheimer's disease affect neurons through various toxic alterations. The aim of this study was to determine the expression of the vitamin D receptor (VDR), 25-hydroxyvitamin D-3 24-hydroxylase (an accelerator of vitamin D catabolism), and the L-type voltage-sensitive calcium channel A1C (LVSCC-A1C) in hippocampal neurons in response to beta amyloid and vitamin D treatments to test the protective effects of vitamin D and the probable effects of beta amyloid on vitamin D catabolism. Methods: The expression of the VDR, 24-hydroxylase (24OHase) and LVSCC-A1C mRNAs were studied using quantitative real-time polymerase chain reaction, and the cytotoxicity levels were determined by an ELISA in primary hippocampal neuron cultures prepared from Sprague-Dawley rat embryos. Results: Our results demonstrated that beta amyloid suppressed the expression of VDR mRNA and induced the expression of 24OHase and LVSCC-A1C mRNAs. Conclusion: Beta amyloid may disrupt the vitamin D-VDR pathway and cause defective utilization of vitamin D by suppressing the level of the VDR and elevating the level of 24OHase. Copyright (C) 2013 S. Karger AG, Basel