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ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism

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ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism. / Furmanik, Malgorzata; Shanahan, Catherine M.

In: BMC Research Notes, 16.07.2018.

Research output: Contribution to journalArticle

Harvard

Furmanik, M & Shanahan, CM 2018, 'ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism', BMC Research Notes. https://doi.org/10.1186/s13104-018-3582-4

APA

Furmanik, M., & Shanahan, C. M. (2018). ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism. BMC Research Notes. https://doi.org/10.1186/s13104-018-3582-4

Vancouver

Furmanik M, Shanahan CM. ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism. BMC Research Notes. 2018 Jul 16. https://doi.org/10.1186/s13104-018-3582-4

Author

Furmanik, Malgorzata ; Shanahan, Catherine M. / ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism. In: BMC Research Notes. 2018.

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@article{60171c4e38fe4f979f9fdb4be06b8e60,
title = "ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism",
abstract = "ObjectiveVascular calcification is the deposition of hydroxyapatite crystals in the blood vessel wall. Osteogenic differentiation of vascular smooth muscle cells (VSMCs) plays a key role in this process. Increased expression of alkaline phosphatase (ALP) occurs in some in vitro models of VSMC calcification and is thought to be crucial for mineralization, however, little is known about the transcriptional regulation of ALP in VSMCs. Recently, ALP upregulation was shown to coincide with endoplasmic reticulum (ER) stress-mediated vascular calcification, specifically with expression of the transcription factor ATF4. As no direct links between ALP expression and ER stress have previously been demonstrated in VSMCs, the aim of this study was to investigate whether ATF4 interacts directly with the ALP promoter.ResultsThe present study shows that ALP mRNA and activity were significantly increased by ER stress treatment of human primary VSMCs in vitro and that this was ATF4-dependent. Bioinformatics analysis predicted two ATF4 binding sites in ER-stress responsive regions of the ALP promoter (− 3631 to − 2048 bp from the first intron). However, we found that ATF4 does not bind within this fragment of the ALP promoter region.",
author = "Malgorzata Furmanik and Shanahan, {Catherine M.}",
year = "2018",
month = "7",
day = "16",
doi = "10.1186/s13104-018-3582-4",
language = "English",
journal = "BMC Research Notes",
issn = "1756-0500",
publisher = "BioMed Central",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - ER stress regulates alkaline phosphatase gene expression in vascular smooth muscle cells via an ATF4-dependent mechanism

AU - Furmanik, Malgorzata

AU - Shanahan, Catherine M.

PY - 2018/7/16

Y1 - 2018/7/16

N2 - ObjectiveVascular calcification is the deposition of hydroxyapatite crystals in the blood vessel wall. Osteogenic differentiation of vascular smooth muscle cells (VSMCs) plays a key role in this process. Increased expression of alkaline phosphatase (ALP) occurs in some in vitro models of VSMC calcification and is thought to be crucial for mineralization, however, little is known about the transcriptional regulation of ALP in VSMCs. Recently, ALP upregulation was shown to coincide with endoplasmic reticulum (ER) stress-mediated vascular calcification, specifically with expression of the transcription factor ATF4. As no direct links between ALP expression and ER stress have previously been demonstrated in VSMCs, the aim of this study was to investigate whether ATF4 interacts directly with the ALP promoter.ResultsThe present study shows that ALP mRNA and activity were significantly increased by ER stress treatment of human primary VSMCs in vitro and that this was ATF4-dependent. Bioinformatics analysis predicted two ATF4 binding sites in ER-stress responsive regions of the ALP promoter (− 3631 to − 2048 bp from the first intron). However, we found that ATF4 does not bind within this fragment of the ALP promoter region.

AB - ObjectiveVascular calcification is the deposition of hydroxyapatite crystals in the blood vessel wall. Osteogenic differentiation of vascular smooth muscle cells (VSMCs) plays a key role in this process. Increased expression of alkaline phosphatase (ALP) occurs in some in vitro models of VSMC calcification and is thought to be crucial for mineralization, however, little is known about the transcriptional regulation of ALP in VSMCs. Recently, ALP upregulation was shown to coincide with endoplasmic reticulum (ER) stress-mediated vascular calcification, specifically with expression of the transcription factor ATF4. As no direct links between ALP expression and ER stress have previously been demonstrated in VSMCs, the aim of this study was to investigate whether ATF4 interacts directly with the ALP promoter.ResultsThe present study shows that ALP mRNA and activity were significantly increased by ER stress treatment of human primary VSMCs in vitro and that this was ATF4-dependent. Bioinformatics analysis predicted two ATF4 binding sites in ER-stress responsive regions of the ALP promoter (− 3631 to − 2048 bp from the first intron). However, we found that ATF4 does not bind within this fragment of the ALP promoter region.

U2 - 10.1186/s13104-018-3582-4

DO - 10.1186/s13104-018-3582-4

M3 - Article

JO - BMC Research Notes

JF - BMC Research Notes

SN - 1756-0500

ER -

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