Evidence map›Paper›PMID 24482492›Full record

ArticleJournal of molecular endocrinology2014

Upregulation of IGF2 expression during vascular calcification.

Dongxing Zhu, Neil C W Mackenzie, Jose Luis Millan, Colin Farquharson, Vicky E Macrae

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023
    Review
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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

5 authors at 1 institution in 2 countries.

Dongxing ZhuThe Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Roslin, Midlothian, EH25 9RG Scotland, UK Sanford-Burnham Medical Research Institute, Sanford Children's Health Research Center, La Jolla, California 92037, USA.
Neil C W Mackenzie
Jose Luis Millan
Colin Farquharson
Vicky E Macrae
University of Edinburgh · GB

Funding

Mechanisms of initiation of skeletal mineralizationR01AR053102 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI MILLAN, JOSE LUIS · 2006 to 2015
$3.8M
Biotechnology and Biological Sciences Research Council BB/F023928/1NIAMS NIH HHS R01 AR053102
6 · The paper itself

Abstract

The process of vascular calcification shares many similarities with that of skeletal mineralisation and involves the deposition of hydroxyapatite crystals in arteries and cardiac valves. However, the cellular mechanisms responsible have yet to be fully elucidated. In this study, we employed microarray analysis to demonstrate the upregulation of more than >9000 genes during the calcification of murine vascular smooth muscle cells (VSMCs), of which the most significantly, differentially expressed gene was Igf2. Following the validation of increased IGF2 expression by RT-qPCR and immunoblotting in calcifying murine VSMCs, IGF2 expression was further demonstrated in the calcified aorta of the Enpp1(-/-) mouse model of medial aortic calcification. Having confirmed that IGF1R and IGF2R were expressed in cultured murine VSMCs, cell-signalling studies in these cells revealed that IGF2 (50 ng/ml) significantly stimulated the phosphorylation of Akt and Erk1/2 (P<0.05). These results potentially indicate that IGF2 may mediate VSMC calcification via the stimulation of Erk1/2 and Akt signalling. This study suggests that the increased IGF2 expression in calcifying VSMCs may reflect the well-established prenatal role of IGF2, particularly as the osteogenic phenotypic transition of VSMCs in a calcified environment recapitulates many of the events occurring during embryonic development. A full understanding of the importance of IGF2 in this pathological process will lead to a better understanding of the aetiology of vascular calcification.

Indexed as

AnimalsAortaDisease Models, AnimalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesGene Expression ProfilingInsulin-Like Growth Factor IIMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphoric Diester HydrolasesProtein KinasesPyrophosphatasesectonucleotide pyrophosphatase phosphodiesterase 1Extracellular Signal-Regulated MAP KinasesInsulin-Like Growth Factor IIPhosphoric Diester HydrolasesProtein KinasesPyrophosphatasesIGF2NPP1vascular calcificationVSMC

Identifiers

PMID24482492
PMCPMC5610348
OpenAlexW2132879053

What OpenQuestion holds

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Registered trials

None linked

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.