Evidence map›Paper›PMID 26887829›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Melanocortin 1 receptor agonist protects podocytes through catalase and RhoA activation.

Johannes Elvin, Lisa Buvall, Annika Lindskog Jonsson, Anna Granqvist, Emelie Lassén, Lovisa Bergwall, Jenny Nyström, Börje Haraldsson

Abstract read
PubMed Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. The podocyte as a direct target for treatment of glomerular disease?American journal of physiology. Renal physiology · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Johannes ElvinDepartment of Molecular and Clinical Medicine, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; johannes.elvin@gu.se.ORCID 0000-0002-9678-9020
Lisa BuvallDepartment of Physiology, Institute of Neuroscience and Physiology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; and Department of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Annika Lindskog JonssonDepartment of Molecular and Clinical Medicine, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;
Anna GranqvistDepartment of Molecular and Clinical Medicine, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;
Emelie LassénDepartment of Molecular and Clinical Medicine, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;
Lovisa BergwallDepartment of Physiology, Institute of Neuroscience and Physiology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; and.
Jenny NyströmDepartment of Physiology, Institute of Neuroscience and Physiology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; and.
Börje HaraldssonDepartment of Molecular and Clinical Medicine, Institute of Medicine, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden;

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drugs containing adrenocorticotropic hormone have been used as therapy for patients with nephrotic syndrome. We have previously shown that adrenocorticotropic hormone and a selective agonist for the melanocortin 1 receptor (MC1R) exert beneficial actions in experimental membranous nephropathy with reduced proteinuria, reduced oxidative stress, and improved glomerular morphology and function. Our hypothesis is that MC1R activation in podocytes elicits beneficial effects by promoting stress fibers and maintaining podocyte viability. To test the hypothesis, we cultured podocytes and used highly specific agonists for MC1R. Podocytes were subjected to the nephrotic-inducing agent puromycin aminonucleoside, and downstream effects of MC1R activation on podocyte survival, antioxidant defense, and cytoskeleton dynamics were studied. To increase the response and enhance intracellular signals, podocytes were transduced to overexpress MC1R. We showed that puromycin promotes MC1R expression in podocytes and that activation of MC1R promotes an increase of catalase activity and reduces oxidative stress, which results in the dephosphorylation of p190RhoGAP and formation of stress fibers through RhoA. In addition, MC1R agonists protect against apoptosis. Together, these mechanisms protect the podocyte against puromycin. Our findings strongly support the hypothesis that selective MC1R-activating agonists protect podocytes and may therefore be useful to treat patients with nephrotic syndromes commonly considered as podocytopathies.

Indexed as

AnimalsAntimetabolitesCatalaseCells, CulturedEnzyme ActivationMiceNephrosisOxidative StressPodocytesPuromycin AminonucleosideReactive Oxygen SpeciesReceptor, Melanocortin, Type 1rhoA GTP-Binding ProteinStress FibersAntimetabolitesCatalasePuromycin AminonucleosideReactive Oxygen SpeciesReceptor, Melanocortin, Type 1rhoA GTP-Binding Proteinactin stress fibermelanocortin 1 receptoroxidative stresspodocyte

Identifiers

PMID26887829

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.