Evidence map›Paper›PMID 30087458›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2018

Lipocalin-2 abrogates epithelial cell cycle arrest by PPARγ inhibition.

Michaela Jung, Bernhard Brüne, Andreas von Knethen, Roser Guiteras, Josep Maria Cruzado, Georgina Hotter, Anna Sola

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Macrophage Phenotype and Fibrosis in Diabetic Nephropathy.International journal of molecular sciences · 2020
    Review
  11. Exploring macrophage cell therapy on Diabetic Kidney Disease.Journal of cellular and molecular medicine · 2019
    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

7 authors at 3 institutions in 2 countries.

Michaela JungInstitute of Biochemistry I, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Bernhard BrüneInstitute of Biochemistry I, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Andreas von KnethenInstitute of Biochemistry I, Goethe-University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany.
Roser GuiterasDepartment of Experimental Nephrology, IDIBELL, L'Hospitalet del Llobregat, Barcelona, Spain.
Josep Maria CruzadoDepartment of Experimental Nephrology, IDIBELL, L'Hospitalet del Llobregat, Barcelona, Spain.
Georgina HotterDepartment of Ischemia and Inflammation, IIBB-CSIC-IDIBAPS, Rosselló, 161, 7th floor, 08036, Barcelona, Spain.
Anna SolaDepartment of Experimental Nephrology, IDIBELL, L'Hospitalet del Llobregat, Barcelona, Spain. asola@idibell.cat.
Goethe University Frankfurt · DEInstitut d'Investigació Biomédica de Bellvitge · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage-epithelial cross-talk regulates cell cycle progression and represents an important factor in rescuing epithelial cells from cell cycle arrest in order to maintain a healthy epithelial phenotype. However, the underlying mechanisms are still not well defined. We provide evidence that macrophage-secreted lipocalin-2 (Lcn-2) plays a key role during this process. In a co-culture setup using cell cycle arrested NRK52e renal epithelial cells and primary bone marrow-derived macrophages, Lcn-2 restores proliferation through inhibition of peroxisome proliferator-activated receptor (PPAR)-γ. Lcn-2 overexpression in macrophages overcomes epithelial cell cycle arrest and enhances epithelial markers via megalin and the downstream activation of PI3K/Akt signalling pathway, whereas a knockdown of Lcn-2 in macrophages prevented this effect. Our results show that macrophage-secreting Lcn-2 is crucial in rescuing epithelial cells from cell cycle arrest and in promoting epithelial proliferation.

Indexed as

Cell ProliferationAnimalsCell CycleCell LineEpithelial CellsLipocalin-2Low Density Lipoprotein Receptor-Related Protein-2MacrophagesPhenotypePhosphatidylinositol 3-KinasesPPAR gammaProto-Oncogene Proteins c-aktRats, Sprague-DawleyLcn2 protein, ratLipocalin-2Low Density Lipoprotein Receptor-Related Protein-2Lrp2 protein, ratPhosphatidylinositol 3-KinasesPPAR gammaProto-Oncogene Proteins c-akt

Identifiers

PMID30087458
OpenAlexW2886602181

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.