Evidence map›Paper›PMID 19692488›Full record

ArticleAmerican journal of physiology. Renal physiology2009

Oxalate-induced activation of PKC-alpha and -delta regulates NADPH oxidase-mediated oxidative injury in renal tubular epithelial cells.

Vijayalakshmi Thamilselvan, Mani Menon, Sivagnanam Thamilselvan

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Article
  8. The metabolomics of a protein kinase C delta (PKCδ) knock-out mouse model.Metabolomics : Official journal of the Metabolomic Society · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Protective Roles of Estrogen ReceptorOxidative medicine and cellular longevity · 2019
    Article
  14. Vitamin D and calcium kidney stones: a review and a proposal.International urology and nephrology · 2019
    Review
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Article
  20. Osteogenic changes in kidneys of hyperoxaluric rats.Biochimica et biophysica acta · 2015
    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

3 authors at 1 institution in 1 country.

Vijayalakshmi ThamilselvanVattikuti Urology Institute, Henry Ford Health System, Detroit, Michigan 48202, USA.
Mani Menon
Sivagnanam Thamilselvan
Henry Ford Health System · US

Funding

UROLITHIASIS AND PEROXIDATIVE INJURYR01DK056249 · NIDDK · UNIVERSITY OF FLORIDA · PI THAMILSELVAN, SIVAGNANAM · 1999 to 2008
$1.5M
NIDDK NIH HHS R01 DK56249
6 · The paper itself

Abstract

Oxalate-induced oxidative stress contributes to cell injury and promotes renal deposition of calcium oxalate crystals. However, we do not know how oxalate stimulates reactive oxygen species (ROS) in renal tubular epithelial cells. We investigated the signaling mechanism of oxalate-induced ROS formation in these cells and found that oxalate significantly increased membrane-associated protein kinase C (PKC) activity while at the same time lowering cytosolic PKC activity. Oxalate markedly translocated PKC-alpha and -delta from the cytosol to the cell membrane. Pretreatment of LLC-PK1 cells with specific inhibitors of PKC-alpha or -delta significantly blocked oxalate-induced generation of superoxide and hydrogen peroxide along with NADPH oxidase activity, LDH release, lipid hydroperoxide formation, and apoptosis. The PKC activator PMA mimicked oxalate's effect on oxidative stress in LLC-PK1 cells as well as cytosol-to-membrane translocation of PKC-alpha and -delta. Silencing of PKC-alpha expression by PKC-alpha-specific small interfering RNA significantly attenuated oxalate-induced cell injury by decreasing hydrogen peroxide generation and LDH release. We believe this is the first demonstration that PKC-alpha- and -delta-dependent activation of NADPH oxidase is one of the mechanisms responsible for oxalate-induced oxidative injury in renal tubular epithelial cells. The study suggests that the therapeutic approach might be considered toward attenuating oxalate-induced PKC signaling-mediated oxidative injury in recurrent stone formers.

Indexed as

AnimalsApoptosisBlotting, WesternElectrophoresis, Polyacrylamide GelEnzyme InhibitorsEpithelial CellsHydrogen PeroxideKidney TubulesLipid PeroxidationL-Lactate DehydrogenaseLLC-PK1 CellsNADPH OxidasesOxalatesOxidative StressProtein Kinase C-alphaProtein Kinase C-deltaEnzyme InhibitorsHydrogen PeroxideL-Lactate DehydrogenaseNADPH OxidasesOxalatesProtein Kinase C-alphaProtein Kinase C-deltaReactive Oxygen Species

Identifiers

PMID19692488
PMCPMC2781341
OpenAlexW2110234303

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.