Evidence map›Paper›PMID 32360782›Full record

ArticleThe ocular surface2020

Eicosapentaenoic acid (EPA) activates PPARγ signaling leading to cell cycle exit, lipid accumulation, and autophagy in human meibomian gland epithelial cells (hMGEC).

Sun Woong Kim, Chang Rae Rho, Jinseor Kim, Yilu Xie, Richard C Prince, Khawla Mustafa, Eric O Potma, Donald J Brown, James V Jester

Open access · greenAbstract read
In one paragraph

Article in The ocular surface, 2020. 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
3.6field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  8. Expression Variation ofInternational journal of molecular sciences · 2023
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  20. Lipid droplets as endogenous intracellular microlenses.Light, science & applications · 2021
    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

9 authors at 2 institutions in 2 countries.

Sun Woong KimDepartment of Ophthalmology, Yonsei University Wonju College of Medicine, Wonju, South Korea.
Chang Rae RhoDepartment of Ophthalmology, Daejeon St Mary Hospital, Daejeon, South Korea; Gavin Herbert Eye Institute, University of California, Irvine, Irvine, CA, USA.
Jinseor KimGavin Herbert Eye Institute, University of California, Irvine, Irvine, CA, USA.
Yilu XieGavin Herbert Eye Institute, University of California, Irvine, Irvine, CA, USA.
Richard C PrinceDepartment of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA.
Khawla MustafaDepartment of Chemistry, University of California, Irvine, Irvine, CA, USA.
Eric O PotmaDepartment of Biomedical Engineering, University of California, Irvine, Irvine, CA, USA; Department of Chemistry, University of California, Irvine, Irvine, CA, USA.
Donald J BrownGavin Herbert Eye Institute, University of California, Irvine, Irvine, CA, USA.
James V JesterGavin Herbert Eye Institute, University of California, Irvine, Irvine, CA, USA. Electronic address: JJester@uci.edu.
University of California, Irvine · USYonsei University · KR

Funding

Age-Related Meibomian Gland DysfunctionR01EY021510 · NEI · UNIVERSITY OF CALIFORNIA-IRVINE · PI James V Jester · 2011 to 2026
$4.8M
High-resolution spectroscopic imaging with infrared nonlinear optical (IR-NLO) microscopyR01GM132506 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI POTMA, ERIC OLAF · 2019 to 2022
$742k
NEI NIH HHS R01 EY021510NIGMS NIH HHS R01 GM132506
6 · The paper itself

Abstract

purposeThe purpose of this study was to access the ability of the natural PPAR agonist, eicosapentaenoic acid (EPA), to activate PPAR gamma (γ) signaling leading to meibocyte differentiation in human meibomian gland epithelial cell (hMGEC).

methodsHMGEC were exposed to EPA, alone and in combination with the specific PPARγ antagonist, T0070907, to selectively block PPARγ signaling. Expression of PPARγ response genes were evaluated by qPCR. Effect on cell cycle was evaluated using Ki-67 labelling and western blots. During differentiation, autophagy was monitored using the Autophagy Tandem Sensor (ATS) and LysoTracker. Lipid accumulation was characterized by Stimulated Raman Scattering microscopy (SRS) and neutral lipid staining in combination with ER-Tracker, LysoTracker, and ATS. Autophagy was also investigated using western blotting. Seahorse XF analysis was performed to monitor mitochondrial function.

resultsEPA specifically upregulated expression of genes related to lipid synthesis and induced cell cycle exit through reduced cyclin D1 expression and increased p21 and p27 expression. EPA also induced accumulation of lipid droplets in a time and dose dependent manner (P < 0.05) by specific PPARγ signaling. Lipid analysis identified both de novo synthesis and extracellular transport of lipid to form lipid droplets that were localized to the ER. PPARγ signaling also induced activation of AMPK-ULK1 signaling and autophagy, while inhibition of autophagy induced mitochondrial crisis with no effect on lipid accumulation.

conclusionsEPA induces meibocyte differentiation through PPARγ activation that is characterized by cell cycle exit, de novo and transported lipid accumulation in the ER, and autophagy.

Indexed as

Epithelial CellsMeibomian GlandsAutophagyCell CycleEicosapentaenoic AcidHumansPPAR gammaEicosapentaenoic AcidPPAR gammaAutophagyCell cycle exitHuman meibomian gland epithelial cellMeibocytePPARγ

Identifiers

PMID32360782
PMCPMC9487759
OpenAlexW3023539544

What OpenQuestion holds

Textmetadata
LicenceTDM
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.