Evidence map›Paper›PMID 29617419›Full record

ArticlePloS one2018

PPAR-gamma activation is associated with reduced liver ischemia-reperfusion injury and altered tissue-resident macrophages polarization in a mouse model.

Ivan Linares, Kaveh Farrokhi, Juan Echeverri, Johan Moritz Kaths, Dagmar Kollmann, Matyas Hamar, Peter Urbanellis, Sujani Ganesh, Oyedele A Adeyi, Paul Yip and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  7. Pioglitazone Modifies Kupffer Cell Function and Protects againstInternational journal of molecular sciences · 2022
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  18. Macrophage Polarization and Liver Ischemia-Reperfusion Injury.International journal of medical sciences · 2021
    Review
  19. Review
  20. 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

12 authors at 2 institutions in 1 country.

Ivan LinaresMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.ORCID 0000-0001-5124-9883
Kaveh FarrokhiMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Juan EcheverriMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Johan Moritz KathsMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Dagmar KollmannMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Matyas HamarMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Peter UrbanellisMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Sujani GaneshMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Oyedele A AdeyiDepartment of Pathology, Toronto General Hospital, Toronto, ON, Canada.
Paul YipLaboratory of Medicine and Pathobiology, Toronto General Hospital, Toronto, ON, Canada.
Markus SelznerMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Nazia SelznerMulti Organ Transplant Program, Toronto General Hospital, Toronto, ON, Canada.
Toronto General Hospital · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPPAR-gamma (γ) is highly expressed in macrophages and its activation affects their polarization. The effect of PPAR-γ activation on Kupffer cells (KCs) and liver ischemia-reperfusion injury (IRI) has not yet been evaluated. We investigated the effect of PPAR-γ activation on KC-polarization and IRI. MATERIALS AND

methodsSeventy percent (70%) liver ischemia was induced for 60mins. PPAR-γ-agonist or vehicle was administrated before reperfusion. PPAR-γ-antagonist was used to block PPAR-γ activation. Liver injury, necrosis, and apoptosis were assessed post-reperfusion. Flow-cytometry determined KC-phenotypes (pro-inflammatory Nitric Oxide +, anti-inflammatory CD206+ and anti-inflammatory IL-10+).

resultsLiver injury assessed by serum AST was significantly decreased in PPAR-γ-agonist versus control group at all time points post reperfusion (1hr: 3092±105 vs 4469±551; p = 0.042; 6hr: 7041±1160 vs 12193±1143; p = 0.015; 12hr: 5746±328 vs 8608±1259; p = 0.049). Furthermore, liver apoptosis measured by TUNEL-staining was significantly reduced in PPAR-γ-agonist versus control group post reperfusion (1hr:2.46±0.49 vs 6.90±0.85%;p = 0.001; 6hr:26.40±2.93 vs 50.13±8.29%; p = 0.048). H&E staining demonstrated less necrosis in PPAR-γ-agonist versus control group (24hr:26.66±4.78 vs 45.62±4.57%; p = 0.032). The percentage of pro-inflammatory NO+ KCs was significantly lower at all post reperfusion time points in the PPAR-γ-agonist versus control group (1hr:28.49±4.99 vs 53.54±9.15%; p = 0.040; 6hr:5.51±0.54 vs 31.12±9.58%; p = 0.009; 24hr:4.15±1.50 vs 17.10±4.77%; p = 0.043). In contrast, percentage of anti-inflammatory CD206+ KCs was significantly higher in PPAR-γ-agonist versus control group prior to IRI (8.62±0.96 vs 4.88 ±0.50%; p = 0.04). Administration of PPAR-γ-antagonist reversed the beneficial effects on AST, apoptosis, and pro-inflammatory NO+ KCs.

conclusionPPAR-γ activation reduces IRI and decreases the pro-inflammatory NO+ Kupffer cells. PPAR-γ activation can become an important tool to improve outcomes in liver surgery through decreasing the pro-inflammatory phenotype of KCs and IRI.

Indexed as

Alanine TransaminaseAnilidesAnimalsApoptosisAspartate AminotransferasesCell PolarityCytokinesDisease Models, AnimalKupffer CellsLectins, C-TypeLiverMaleMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BL2-chloro-5-nitrobenzanilideAlanine TransaminaseAnilidesAspartate AminotransferasesCytokinesLectins, C-TypeMannose-Binding LectinsMannose ReceptorNitric OxidePPAR gammaReceptors, Cell SurfaceRosiglitazoneThiazolidinediones

Identifiers

PMID29617419
PMCPMC5884549
OpenAlexW2796132488

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.