Evidence map›Paper›PMID 23012375›Full record

ArticleThe Journal of biological chemistry2012

Vitamin D suppression of endoplasmic reticulum stress promotes an antiatherogenic monocyte/macrophage phenotype in type 2 diabetic patients.

Amy E Riek, Jisu Oh, Jennifer E Sprague, Alexandra Timpson, Lisa de las Fuentes, Leon Bernal-Mizrachi, Kenneth B Schechtman, Carlos Bernal-Mizrachi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 5% 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

62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Vitamin D and Ocular Diseases: A Systematic Review.International journal of molecular sciences · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Vitamin DThe Journal of steroid biochemistry and molecular biology · 2018
    Trial
  6. Article
  7. Comparative evaluation of the modulatory role of 1,25-dihydroxy-vitamin DJournal of animal science and biotechnology · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. 1,25-dihydroxyvitamin DNutrition research and practice · 2024
    Article
  12. Effects of anNutrition research and practice · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Amy E RiekDivision of Endocrinology, Metabolism, and Lipid Research, Washington University, St. Louis, Missouri 63110, USA.
Jisu Oh
Jennifer E Sprague
Alexandra Timpson
Lisa de las Fuentes
Leon Bernal-Mizrachi
Kenneth B Schechtman
Carlos Bernal-Mizrachi
Washington University in St. Louis · USEmory University · US

Funding

Washington University Institute of Clinical and Translational Sciences (UL1)UL1RR024992 · NCRR · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2007 to 2011
$45.4M
Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
Washington University Institute of Clinical and Translational SciencesKL2TR000450 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$8.8M
Training of the Pediatric Physician-ScientistT32HD043010 · NICHD · WASHINGTON UNIVERSITY · PI MARK E. LOWE · 2002 to 2026
$6.4M
VITAMIN D DEFICIENCY, INSULIN RESISTANCE AND CARDIOVASCULAR DISEASER01HL094818 · NHLBI · WASHINGTON UNIVERSITY · PI Carlos Bernal-Mizrachi · 2010 to 2026
$6.3M
Washington University Center for Kidney Disease ResearchP30DK079333 · NIDDK · WASHINGTON UNIVERSITY · PI HAMMERMAN, MARC RANDALL · 2007 to 2011
$5.1M
NCATS NIH HHS KL2 TR000450NCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1TR000448/KL2TR000450NCRR NIH HHS UL1 RR024992NCRR NIH HHS UL1RR024992/KL2RR024994NHLBI NIH HHS R01 HL094818NHLBI NIH HHS R01HL094818-0NICHD NIH HHS 2 T32 HD043010NIDDK NIH HHS P30 DK079333NIDDK NIH HHS P30DK079333
6 · The paper itself

Abstract

Cardiovascular disease is the leading cause of morbidity/mortality in patients with type 2 diabetes mellitus (T2DM), but there is a lack of knowledge about the mechanism(s) of increased atherosclerosis in these patients. In patients with T2DM, the prevalence of 25-hydroxy vitamin D (25(OH)D) deficiency is almost twice that for nondiabetics and doubles the relative risk of developing cardiovascular disease compared with diabetic patients with normal 25(OH)D. We tested the hypothesis that monocytes from vitamin D-deficient subjects will have a proatherogenic phenotype compared with vitamin D-sufficient subjects in 43 patients with T2DM. Serum 25(OH)D level inversely correlated with monocyte adhesion to endothelial cells even after adjustment for demographic and comorbidity characteristics. Vitamin D-sufficient patients (≥30 ng/ml 25(OH)D) had lower monocyte endoplasmic reticulum (ER) stress, a predominance of M1 over M2 macrophage membrane receptors, and decreased mRNA expression of monocyte adhesion molecules PSGL-1, β(1)-integrin, and β(2)-integrin compared with patients with 25(OH)D levels of <30 ng/ml. In vitamin D-deficient macrophages, activation of ER stress increased adhesion and adhesion molecule expression and induced an M2-predominant phenotype. Moreover, adding 1,25(OH)(2)D(3) to vitamin D-deficient macrophages shifted their phenotype toward an M1-predominant phenotype with suppressed adhesion. Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients activated ER stress, accelerated adhesion, and increased adhesion molecule expression. The absence of ER stress protein CCAAT enhancer-binding protein homologous protein suppressed monocyte adhesion, adhesion molecule expression, and the M2-predominant phenotype induced by vitamin D deficiency. Thus, vitamin D is a natural ER stress reliever that induced an antiatherogenic monocyte/macrophage phenotype.

Indexed as

AdultAgedAtherosclerosisCD18 AntigensCell AdhesionCell DifferentiationCross-Sectional StudiesDiabetes Mellitus, Type 2Endoplasmic ReticulumFemaleHumansIntegrin beta1MacrophagesMaleMembrane GlycoproteinsMiddle AgedCD18 AntigensIntegrin beta1Membrane GlycoproteinsP-selectin ligand proteinRNA, MessengerRNA, Small InterferingVitamin D

Identifiers

PMID23012375
PMCPMC3493893
OpenAlexW1979721564

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.