Evidence map›Paper›PMID 22467332›Full record

ArticleInternational journal of cancer2012

Mice lacking epidermal PPARγ exhibit a marked augmentation in photocarcinogenesis associated with increased UVB-induced apoptosis, inflammation and barrier dysfunction.

Ravi P Sahu, Sonia C DaSilva, Badri Rashid, Kellie Clay Martel, Danielle Jernigan, Shama R Mehta, Deena R Mohamed, Samin Rezania, Joshua R Bradish, Andrew B Armstrong and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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  16. Peroxisome proliferator activating receptor-γ and the podocyte.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Review
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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.

Ravi P SahuDepartment of Dermatology, Indiana University School of Medicine, Indianapolis, IN, USA.
Sonia C DaSilva
Badri Rashid
Kellie Clay Martel
Danielle Jernigan
Shama R Mehta
Deena R Mohamed
Samin Rezania
Joshua R Bradish
Andrew B Armstrong
Simon Warren
Raymond L Konger
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

Platelet Activating Factor and Epidermic CytotoxicityR01HL062996 · NHLBI · WRIGHT STATE UNIVERSITY · PI TRAVERS, JEFFREY B. · 1999 to 2023
$7.2M
Tumor Suppression Through Oxidized GlycerophosphocholinesR21ES017497 · NIEHS · INDIANA UNIVERSITY INDIANAPOLIS · PI KONGER, RAYMOND L · 2009 to 2010
$435k
Role of PPARgamma in ultraviolet stress responsesR03AR053710 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KONGER, RAYMOND L · 2007 to 2008
$150k
NHLBI NIH HHS R01 HL062996NIAMS NIH HHS R03 AR053710NIEHS NIH HHS R21 ES017497
6 · The paper itself

Abstract

Recent studies suggest that peroxisome proliferator-activated receptor gamma (PPARγ) agonists may have cancer chemopreventive activity. Other studies have shown that loss of epidermal PPARγ results in enhanced chemical carcinogenesis in mice via unknown mechanisms. However, ultraviolet B (UVB) exposure represents the primary etiological agent for skin cancer formation and the role of PPARγ in photobiology and photocarcinogenesis is unknown. In previous studies, we demonstrated that UVB irradiation of cells results in the formation of oxidized glycerophosphocholines that exhibit PPARγ ligand activity. We therefore hypothesized that PPARγ would prove to be a chemopreventive target in photocarcinogenesis. We first showed that UVB irradiation of mouse skin causes generation of PPARγ agonist species in vivo. We then generated SKH-1 hairless, albino mice deficient in epidermal Pparg (Pparg-/-(epi)) using a cytokeratin 14 driven Cre-LoxP strategy. Using a chronic model of UVB photocarcinogenesis, we next showed that Pparg-/-(epi) mice exhibit an earlier onset of tumor formation, increased tumor burden and tumor progression. Increased tumor burden in Pparg-/-(epi) mice was accompanied by a significant increase in epidermal hyperplasia and p53 positive epidermal cells in surrounding skin lacking tumors. After acute UVB irradiation, Pparg-/-(epi) mice exhibited an augmentation of both UVB-induced Caspase 3/7 activity and inflammation. Increased apoptosis and inflammation was also observed after treatment with the PPARγ antagonist GW9662. With chronic UVB irradiation, Pparg-/-(epi) mice exhibited a sustained increase in erythema and transepidermal water loss relative to wildtype littermates. This suggests that PPARγ agonists could have possible chemopreventive activity in non-melanoma skin cancer.

Indexed as

Cell Transformation, NeoplasticAnimalsApoptosisCaspase 3Caspase 7EpidermisErythemaFemaleHyperplasiaInflammationKeratinocytesLigandsMiceMice, HairlessMice, KnockoutPPAR gammaCaspase 3Caspase 7LigandsPPAR gammaTumor Suppressor Protein p53

Identifiers

PMID22467332
PMCPMC4280796
OpenAlexW2008549124

What OpenQuestion holds

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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.