Evidence map›Paper›PMID 26491046›Full record

ArticleAmerican journal of physiology. Cell physiology2016

Nitrotyrosine impairs mitochondrial function in fetal lamb pulmonary artery endothelial cells.

Ru-Jeng Teng, Tzong-Jin Wu, Adeleye J Afolayan, Girija G Konduri

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Workshop on Synergies Between Alzheimer's Research and Clinical Gerontology and Geriatrics: Current Status and Future Directions.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Review
  7. Review
  8. Article
  9. Article
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

4 authors at 1 institution in 1 country.

Ru-Jeng TengDepartment of Pediatrics, Medical College of Wisconsin, Wauwatosa, Wisconsin rteng@mcw.edu.
Tzong-Jin WuDepartment of Pediatrics, Medical College of Wisconsin, Wauwatosa, Wisconsin.
Adeleye J AfolayanDepartment of Pediatrics, Medical College of Wisconsin, Wauwatosa, Wisconsin.
Girija G KonduriDepartment of Pediatrics, Medical College of Wisconsin, Wauwatosa, Wisconsin.
Medical College of Wisconsin · US

Funding

Clincal and Translational Science AwardUL1TR000055 · NCATS · MEDICAL COLLEGE OF WISCONSIN · PI SHAKER, REZA NONE · 2012 to 2015
$11.3M
REGULATION OF PULMONARY CIRCULATION IN FETUS AND NEWBORNR01HL057268 · NHLBI · WAYNE STATE UNIVERSITY · PI KONDURI, GIRIJA G. · 1998 to 2013
$2.0M
Akt-mediated phosphorylation of hsp70 regulates mitochondrial localization of SOD2 and oxidative stress in pulmonary artery endothelial cells during postnatal transitionK08HL133379 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI AFOLAYAN, ADELEYE J · 2016 to 2021
$821k
Oxidative stress in pulmonary circulation during birth related transitionR03HD065841 · NICHD · MEDICAL COLLEGE OF WISCONSIN · PI KONDURI, GIRIJA G. · 2010 to 2011
$150k
BH4 in hyperoxic lung injury in newbornR03HD073274 · NICHD · MEDICAL COLLEGE OF WISCONSIN · PI TENG, RU-JENG · 2012 to 2013
$149k
NCATS NIH HHS UL1TR000055NHLBI NIH HHS K08 HL133379NHLBI NIH HHS R01-HL-057268NICHD NIH HHS R03-HD-073274NICHD NIH HHS R03-HD-65841
6 · The paper itself

Abstract

Nitration of both protein-bound and free tyrosine by reactive nitrogen species results in the formation of nitrotyrosine (NT). We previously reported that free NT impairs microtubule polymerization and uncouples endothelial nitric oxide synthase (eNOS) function in pulmonary artery endothelial cells (PAEC). Because microtubules modulate mitochondrial function, we hypothesized that increased NT levels during inflammation and oxidative stress will lead to mitochondrial dysfunction in PAEC. PAEC isolated from fetal lambs were exposed to varying concentrations of free NT. At low concentrations (1-10 μM), NT increased nitration of mitochondrial electron transport chain (ETC) protein subunit complexes I-V and state III oxygen consumption. Higher concentrations of NT (50 μM) caused decreased microtubule acetylation, impaired eNOS interactions with mitochondria, and decreased ETC protein levels. We also observed increases in heat shock protein-90 nitration, mitochondrial superoxide formation, and fragmentation of mitochondria in PAEC. Our data suggest that free NT accumulation may impair microtubule polymerization and exacerbate reactive oxygen species-induced cell damage by causing mitochondrial dysfunction.

Indexed as

AcetylationAnimalsCells, CulturedDNA, MitochondrialDose-Response Relationship, DrugElectron Transport Chain Complex ProteinsEndothelial CellsGestational AgeHSP90 Heat-Shock ProteinsMicrotubulesMitochondriaNitric Oxide Synthase Type IIIOxygen ConsumptionProtein BindingPulmonary ArterySheep3-nitrotyrosineDNA, MitochondrialElectron Transport Chain Complex ProteinsHSP90 Heat-Shock ProteinsNitric Oxide Synthase Type IIISuperoxidesTyrosinebioenergeticsmicrotubulesmitochondrianitric oxide

Identifiers

PMID26491046
PMCPMC4698449
OpenAlexW2174534783

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.