Evidence map›Paper›PMID 30012221›Full record

ArticleBMC research notes2018

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

Malgorzata Furmanik, Catherine M Shanahan

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Malgorzata FurmanikCardiovascular Division, James Black Centre, King's College London, 125 Coldharbour Lane, London, SE5 9NU, UK.
Catherine M ShanahanCardiovascular Division, James Black Centre, King's College London, 125 Coldharbour Lane, London, SE5 9NU, UK. cathy.shanahan@kcl.ac.uk.ORCID http://orcid.org/0000-0002-8352-8171
King's College London · GB

Funding

British Heart Foundation FS/11/9/28695
6 · The paper itself

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.

Indexed as

Endoplasmic Reticulum StressActivating Transcription Factor 4Alkaline PhosphataseCells, CulturedHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteogenesisActivating Transcription Factor 4Alkaline PhosphataseATF4 protein, humanAlkaline phosphataseATF4Endoplasmic reticulum stressPromoterVascular smooth muscle cell

Identifiers

PMID30012221
PMCPMC6048897
OpenAlexW2883204900

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.