Evidence map›Paper›PMID 26949104›Full record

ArticleThe Journal of steroid biochemistry and molecular biology2016

1,25(OH)2D3 inhibits oxidative stress and monocyte adhesion by mediating the upregulation of GCLC and GSH in endothelial cells treated with acetoacetate (ketosis).

Preeti Kanikarla-Marie, Sushil K Jain

Abstract read
In one paragraph

Article in The Journal of steroid biochemistry and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 73 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 1 country.

Preeti Kanikarla-MarieDepartments of Pediatrics and Biochemistry & Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA.
Sushil K JainDepartments of Pediatrics and Biochemistry & Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, USA. Electronic address: sjain@lsuhsc.edu.
Louisiana State University Health Sciences Center Shreveport · US

Funding

Ketosis, Vascular Inflammation and Its Therapy in Type 1 Diabetic PatientsR01DK072433 · NIDDK · LOUISIANA STATE UNIV HSC SHREVEPORT · PI JAIN, SUSHIL K · 2007 to 2010
$1.3M
L-cysteine, PIP3 and Insulin Signaling in DiabetesR01AT007442 · NCCIH · LOUISIANA STATE UNIV HSC SHREVEPORT · PI JAIN, SUSHIL K · 2014 to 2015
$643k
NCCIH NIH HHS R01 AT007442NIDDK NIH HHS R01 DK072433
6 · The paper itself

Abstract

backgroundThere is a significantly higher incidence of cardiovascular disease (CVD) among type 1 diabetic (T1D) patients than among non-diabetic subjects. T1D is associated with hyperketonemia, a condition with elevated blood levels of ketones, in addition to hyperglycemia. The biochemical mechanism by which vitamin D (VD) may reduce the risk of CVD is not known. This study examines whether VD can be beneficial in reducing hyperketonemia (acetoacetate, AA) induced oxidative stress in endothelial cells.

methodsHUVEC were pretreated with 1,25(OH)2D3, and later exposed to the ketone body acetoacetate.

resultsThe increases in ROS production, ICAM-1 expression, MCP-1 secretion, and monocyte adhesion in HUVEC treated with AA were significantly reduced following treatment with 1,25(OH)2D3. Interestingly, an increase in glutathione (GSH) levels was also observed with 1,25(OH)2D3 in ketone treated cells. The effects of 1,25(OH)2D3 on GSH, ROS, and monocyte-endothelial adhesion were prevented in GCLC knockdown HUVEC. This suggests that 1,25(OH)2D3 inhibits ROS, MCP-1, ICAM-1, and adherence of monocytes mediated by the upregulation of GCLC and GSH.

conclusionThis study provides evidence for the biochemical mechanism through which VD supplementation may reduce the excess monocyte adhesion to endothelium and inflammation associated with T1D.

Indexed as

AcetoacetatesCalcitriolCell AdhesionCell LineCytokinesDrug Evaluation, PreclinicalGlutamate-Cysteine LigaseGlutathioneHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1KetosisMonocytesOxidative StressReceptors, CalcitriolUp-RegulationAcetoacetatesacetoacetic acidCalcitriolCytokinesGCLC protein, humanGlutamate-Cysteine LigaseGlutathioneIntercellular Adhesion Molecule-1Receptors, Calcitriol1,25(OH)(2)D3EndotheliumKetonesOxidative stressType 1 diabetesVitamin D

Identifiers

PMID26949104
PMCPMC4825694
OpenAlexW2290409696

What OpenQuestion holds

Textmetadata
LicenceTDM
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.