The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.

<h4>Background</h4>Recent studies have suggested that vitamin D can act on cells in the nervous system. Associations between polymorphisms in the vitamin D receptor (VDR), age-dependent cognitive decline, and insufficient serum 25 hydroxyvitamin D(3) levels in Alzheimer's patients a...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Duygu Gezen-Ak, Erdinç Dursun, Selma Yilmazer
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2011
Materias:
R
Q
Acceso en línea:https://doaj.org/article/d2d1b447a8e4427597733e0da5d365d1
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:d2d1b447a8e4427597733e0da5d365d1
record_format dspace
spelling oai:doaj.org-article:d2d1b447a8e4427597733e0da5d365d12021-11-18T06:57:48ZThe effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.1932-620310.1371/journal.pone.0017553https://doaj.org/article/d2d1b447a8e4427597733e0da5d365d12011-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21408608/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Recent studies have suggested that vitamin D can act on cells in the nervous system. Associations between polymorphisms in the vitamin D receptor (VDR), age-dependent cognitive decline, and insufficient serum 25 hydroxyvitamin D(3) levels in Alzheimer's patients and elderly people with cognitive decline have been reported. We have previously shown that amyloid β (Aβ) treatment eliminates VDR protein in cortical neurons. These results suggest a potential role for vitamin D and vitamin D-mediated mechanisms in Alzheimer's disease (AD) and neurodegeneration. Vitamin D has been shown to down-regulate the L-type voltage-sensitive calcium channels, LVSCC-A1C and LVSCC-A1D, and up-regulate nerve growth factor (NGF). However, expression of these proteins when VDR is repressed is unknown. The aim of this study is to investigate LVSCC-A1C, LVSCC-A1D expression levels and NGF release in VDR-silenced primary cortical neurons prepared from Sprague-Dawley rat embryos.<h4>Methodology/principal findings</h4>qRT-PCR and western blots were performed to determine VDR, LVSCC-A1C and -A1D expression levels. NGF and cytotoxicity levels were determined by ELISA. Apoptosis was determined by TUNEL. Our findings illustrate that LVSCC-A1C mRNA and protein levels increased rapidly in cortical neurons when VDR is down-regulated, whereas, LVSCC-A1D mRNA and protein levels did not change and NGF release decreased in response to VDR down-regulation. Although vitamin D regulates LVSCC-A1C through VDR, it may not regulate LVSCC-A1D through VDR.<h4>Conclusions/significance</h4>Our results indicate that suppression of VDR disrupts LVSCC-A1C and NGF production. In addition, when VDR is suppressed, neurons could be vulnerable to aging and neurodegeneration, and when combined with Aβ toxicity, it is possible to explain some of the events that occur during neurodegeneration.Duygu Gezen-AkErdinç DursunSelma YilmazerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 3, p e17553 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Duygu Gezen-Ak
Erdinç Dursun
Selma Yilmazer
The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
description <h4>Background</h4>Recent studies have suggested that vitamin D can act on cells in the nervous system. Associations between polymorphisms in the vitamin D receptor (VDR), age-dependent cognitive decline, and insufficient serum 25 hydroxyvitamin D(3) levels in Alzheimer's patients and elderly people with cognitive decline have been reported. We have previously shown that amyloid β (Aβ) treatment eliminates VDR protein in cortical neurons. These results suggest a potential role for vitamin D and vitamin D-mediated mechanisms in Alzheimer's disease (AD) and neurodegeneration. Vitamin D has been shown to down-regulate the L-type voltage-sensitive calcium channels, LVSCC-A1C and LVSCC-A1D, and up-regulate nerve growth factor (NGF). However, expression of these proteins when VDR is repressed is unknown. The aim of this study is to investigate LVSCC-A1C, LVSCC-A1D expression levels and NGF release in VDR-silenced primary cortical neurons prepared from Sprague-Dawley rat embryos.<h4>Methodology/principal findings</h4>qRT-PCR and western blots were performed to determine VDR, LVSCC-A1C and -A1D expression levels. NGF and cytotoxicity levels were determined by ELISA. Apoptosis was determined by TUNEL. Our findings illustrate that LVSCC-A1C mRNA and protein levels increased rapidly in cortical neurons when VDR is down-regulated, whereas, LVSCC-A1D mRNA and protein levels did not change and NGF release decreased in response to VDR down-regulation. Although vitamin D regulates LVSCC-A1C through VDR, it may not regulate LVSCC-A1D through VDR.<h4>Conclusions/significance</h4>Our results indicate that suppression of VDR disrupts LVSCC-A1C and NGF production. In addition, when VDR is suppressed, neurons could be vulnerable to aging and neurodegeneration, and when combined with Aβ toxicity, it is possible to explain some of the events that occur during neurodegeneration.
format article
author Duygu Gezen-Ak
Erdinç Dursun
Selma Yilmazer
author_facet Duygu Gezen-Ak
Erdinç Dursun
Selma Yilmazer
author_sort Duygu Gezen-Ak
title The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
title_short The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
title_full The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
title_fullStr The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
title_full_unstemmed The effects of vitamin D receptor silencing on the expression of LVSCC-A1C and LVSCC-A1D and the release of NGF in cortical neurons.
title_sort effects of vitamin d receptor silencing on the expression of lvscc-a1c and lvscc-a1d and the release of ngf in cortical neurons.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/d2d1b447a8e4427597733e0da5d365d1
work_keys_str_mv AT duygugezenak theeffectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
AT erdincdursun theeffectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
AT selmayilmazer theeffectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
AT duygugezenak effectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
AT erdincdursun effectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
AT selmayilmazer effectsofvitamindreceptorsilencingontheexpressionoflvscca1candlvscca1dandthereleaseofngfincorticalneurons
_version_ 1718424135185465344