Evidence map›Paper›PMID 27521420›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Vascular smooth muscle cell contractile protein expression is increased through protein kinase G-dependent and -independent pathways by glucose-6-phosphate dehydrogenase inhibition and deficiency.

Sukrutha Chettimada, Sachindra Raj Joshi, Vidhi Dhagia, Alessandro Aiezza, Thomas M Lincoln, Rakhee Gupte, Joseph M Miano, Sachin A Gupte

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. 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
0.9field-weighted citation impact, top 23% 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, 26 citations in OpenAlex.

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  14. Signaling and metabolic properties of fast and slow smooth muscle types from mice.Pflugers Archiv : European journal of physiology · 2018
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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

8 authors at 3 institutions in 1 country.

Sukrutha ChettimadaBiochemistry & Molecular Biology, University of South Alabama, Mobile, Alabama; Pharmacology, New York Medical College, Valhalla, New York.
Sachindra Raj JoshiBiochemistry & Molecular Biology, University of South Alabama, Mobile, Alabama; Pharmacology, New York Medical College, Valhalla, New York.
Vidhi DhagiaPharmacology, New York Medical College, Valhalla, New York.
Alessandro AiezzaAab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.
Thomas M LincolnPhysiology, University of South Alabama, Mobile, Alabama.
Rakhee GupteBiochemistry & Molecular Biology, University of South Alabama, Mobile, Alabama; Pharmacology, New York Medical College, Valhalla, New York.
Joseph M MianoAab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York; and.
Sachin A GupteBiochemistry & Molecular Biology, University of South Alabama, Mobile, Alabama; Pharmacology, New York Medical College, Valhalla, New York.
New York Medical College · USUniversity of South Alabama · USUniversity of Rochester · US

Funding

Regulation of Vascular Smooth Muscle Cell Phenotype by a Novel Isoform of Glucose-6-Phosphate DehydrogenaseR01HL132574 · NHLBI · NEW YORK MEDICAL COLLEGE · PI GUPTE, SACHIN A, MIANO, JOSEPH M · 2017 to 2020
$2.5M
NHLBI NIH HHS R01 HL132574
6 · The paper itself

Abstract

Homeostatic control of vascular smooth muscle cell (VSMC) differentiation is critical for contractile activity and regulation of blood flow. Recently, we reported that precontracted blood vessels are relaxed and the phenotype of VSMC is regulated from a synthetic to contractile state by glucose-6-phosphate dehydrogenase (G6PD) inhibition. In the current study, we investigated whether the increase in the expression of VSMC contractile proteins by inhibition and knockdown of G6PD is mediated through a protein kinase G (PKG)-dependent pathway and whether it regulates blood pressure. We found that the expression of VSMC-restricted contractile proteins, myocardin (MYOCD), and miR-1 and miR-143 are increased by G6PD inhibition or knockdown. Importantly, RNA-sequence analysis of aortic tissue from G6PD-deficient mice revealed uniform increases in VSMC-restricted genes, particularly those regulated by the MYOCD-serum response factor (SRF) switch. Conversely, expression of Krüppel-like factor 4 (KLF4) is decreased by G6PD inhibition. Interestingly, the G6PD inhibition-induced expression of miR-1 and contractile proteins was blocked by Rp-β-phenyl-1,N

Indexed as

AnimalsAortaBlotting, WesternCattleChromatography, LiquidContractile ProteinsCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IGene Knockdown TechniquesGlucosephosphate DehydrogenaseImmunoprecipitationKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMicroRNAsMuscle, Smooth, VascularContractile ProteinsCyclic GMP-Dependent Protein KinasesCyclic GMP-Dependent Protein Kinase Type IGlucosephosphate DehydrogenaseKlf4 protein, mouseKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN143 microRNA, mouseMirn1 microRNA, mouseMyocardinNuclear ProteinsSerum Response FactorTrans-ActivatorsepigeneticsmetabolismNADPH redoxpentose phosphate pathwayprotein kinase GRNA-seqvascular smooth muscle phenotype

Identifiers

PMID27521420
PMCPMC5114469
OpenAlexW2525920590

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.