Evidence map›Paper›PMID 18390927›Full record

ArticleJournal of leukocyte biology2008

Priming of neutrophil oxidative burst in diabetes requires preassembly of the NADPH oxidase.

Kazuhiro Omori, Taisuke Ohira, Yushi Uchida, Srinivas Ayilavarapu, Eraldo L Batista, Motohiko Yagi, Tomoyuki Iwata, Hongsheng Liu, Hatice Hasturk, Alpdogan Kantarci and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 136 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

11 authors at 1 institution in 1 country.

Kazuhiro OmoriDepartment of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, 100 East Newton Street, Suite 107, Boston, MA 02118, USA.
Taisuke Ohira
Yushi Uchida
Srinivas Ayilavarapu
Eraldo L Batista
Motohiko Yagi
Tomoyuki Iwata
Hongsheng Liu
Hatice Hasturk
Alpdogan Kantarci
Thomas E Van Dyke
Boston University · US

Funding

YOGA INDUCED CHANGES IN BRAIN GABA LEVELSM01RR000533 · NCRR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HOLICK, MICHAEL F. · 1985 to 2008
$19.4M
Neutrophils and Periodontitis in DiabetesR01DE015566 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI VAN DYKE, THOMAS ELLIOTT · 2005 to 2014
$4.2M
In vivo study of diabetic hyperglycemia and inflammationR01DE016933 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GYURKO, ROBERT · 2005 to 2009
$1.3M
NCRR NIH HHS M01 RR000533NCRR NIH HHS RR-00533NIDCR NIH HHS DE-15566NIDCR NIH HHS DE-16933NIDCR NIH HHS R01 DE015566NIDCR NIH HHS R01 DE016933
6 · The paper itself

Abstract

Hyperglycemia associated with diabetes mellitus results in the priming of neutrophils leading to oxidative stress that is, in part, responsible for diabetic complications. p47phox, a NADPH oxidase cytosolic subunit, is a key protein in the assembly of the NADPH oxidase leading to superoxide generation. Little is known about the priming mechanism of oxidative pathways in neutrophils of people with diabetes. In this study, the kinetics of p47phox activation was investigated by comparing neutrophils from diabetic and healthy subjects, and the mechanism of hyperglycemia-induced changes was studied by using neutrophil-like HL-60 cells as a model. In resting neutrophils from diabetic subjects, p47phox prematurely translocates to the cell membrane and preassembles with p22phox, a NADPH oxidase membrane subunit. This premature p47phox translocation and preassembly with p22phox were also observed in HL-60 cells cultured with high glucose (HG; 25 mM) and with the specific ligand for the receptor for advanced glycation end products (RAGE), S100B. Phosphorylation of ERK1/2, but not p38 MAPK, was the primary signaling pathway, as evidenced by PD98059 suppressing the translocation of p47phox in HL-60 cells incubated with HG and S100B. HL-60 cells cultured in HG and S100B exhibited a 1.8-fold increase in fMLP-induced superoxide generation compared with those cultured in normal glucose (5.5 mM). These data suggest that HG and increased AGE prime neutrophils and increase oxidative stress inducing the translocation of p47phox to the cell membrane and preassembly with p22phox by stimulating a RAGE-ERK1/2 pathway.

Indexed as

Respiratory BurstAdultCell MembraneDiabetes MellitusFemaleFlavonoidsHL-60 CellsHumansMaleMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH OxidasesNeutrophilsN-Formylmethionine Leucyl-PhenylalanineOxidative Stressp38 Mitogen-Activated Protein Kinases2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneCYBA protein, humanFlavonoidsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NADPH Oxidasesneutrophil cytosolic factor 1N-Formylmethionine Leucyl-Phenylalaninep38 Mitogen-Activated Protein KinasesReceptor for Advanced Glycation End ProductsReceptors, ImmunologicSuperoxides

Identifiers

PMID18390927
PMCPMC2774791
OpenAlexW2118473348

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.