Evidence map›Paper›PMID 24135074›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

A novel and potent inhibitor of dimethylarginine dimethylaminohydrolase: a modulator of cardiovascular nitric oxide.

Yohannes T Ghebremariam, Daniel A Erlanson, John P Cooke

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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

3 authors at 2 institutions in 1 country.

Yohannes T GhebremariamDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, Texas (Y.T.G., J.P.C.); and SPARK Translational Research Program, Stanford University, School of Medicine, Stanford, California (D.A.E.).
Daniel A Erlanson
John P Cooke
Stanford University · USHouston Methodist · US

Funding

Basic and Translational Research iPSC-based hematologic and vascular therapiesU01HL100397 · NHLBI · STANFORD UNIVERSITY · PI COOKE, JOHN P · 2009 to 2015
$7.4M
Stanford Career Development in Vascular MedicineK12HL087746 · NHLBI · STANFORD UNIVERSITY · PI DALMAN, RONALD L · 2007 to 2012
$3.5M
DDAH As a Novel Target in Pulmonary FibrosisK01HL118683 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI GHEBRE, YOHANNES T · 2013 to 2017
$682k
NHLBI NIH HHS 1K01HL118683-01NHLBI NIH HHS 1U01HL100397NHLBI NIH HHS K01 HL118683NHLBI NIH HHS K12 HL087746NHLBI NIH HHS K12HL087746NHLBI NIH HHS U01 HL100397
6 · The paper itself

Abstract

PD 404182 [6H-6-imino-(2,3,4,5-tetrahydropyrimido)[1,2-c]-[1,3]benzothiazine], a heterocyclic iminobenzothiazine derivative, is a member of the Library of Pharmacologically Active Compounds (LOPAC) that is reported to possess antimicrobial and anti-inflammatory properties. In this study, we used biochemical assays to screen LOPAC against human dimethylarginine dimethylaminohydrolase isoform 1 (DDAH1), an enzyme that physiologically metabolizes asymmetric dimethylarginine (ADMA), an endogenous and competitive inhibitor of nitric oxide (NO) synthase. We discovered that PD 404182 directly and dose-dependently inhibits DDAH. Moreover, PD 404182 significantly increased intracellular levels of ADMA in cultured primary human vascular endothelial cells (ECs) and reduced lipopolysaccharide-induced NO production in these cells, suggesting its therapeutic potential in septic shock-induced vascular collapse. In addition, PD 404182 abrogated the formation of tube-like structures by ECs in an in vitro angiogenesis assay, indicating its antiangiogenic potential in diseases characterized by pathologically excessive angiogenesis. Furthermore, we investigated the potential mechanism of inhibition of DDAH by this small molecule and found that PD 404182, which has striking structural similarity to ADMA, could be competed by a DDAH substrate, suggesting that it is a competitive inhibitor. Finally, our enzyme kinetics assay showed time-dependent inhibition, and our inhibitor dilution assay showed that the enzymatic activity of DDAH did not recover significantly after dilution, suggesting that PD 404182 might be a tightly bound, covalent, or an irreversible inhibitor of human DDAH1. This proposal is supported by mass spectrometry studies with PD 404182 and glutathione.

Indexed as

AmidohydrolasesCells, CulturedEndothelium, VascularFemaleHumansHydroxamic AcidsIminesNeovascularization, PathologicNitric OxideNitric Oxide SynthaseThiazinesVorinostat6H-6-imino-(2,3,4,5-tetrahydropyrimido)(1,2-c)-(1,3)benzothiazineAmidohydrolasesdimethylargininaseHydroxamic AcidsIminesNitric OxideNitric Oxide SynthaseThiazinesVorinostat

Identifiers

PMID24135074
PMCPMC3868884
OpenAlexW2147414463

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.