Evidence map›Paper›PMID 25962726›Full record

ArticleBMC immunology2015

Targeting epidermal fatty acid binding protein for treatment of experimental autoimmune encephalomyelitis.

Enyu Rao, Puja Singh, Yan Li, Yuwen Zhang, Young-In Chi, Jill Suttles, Bing Li

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

Article in BMC immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Enyu RaoThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. erao@hi.umn.edu.
Puja SinghThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. psingh@hi.umn.edu.
Yan LiThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. yli@hi.umn.edu.
Yuwen ZhangThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. yzhang@hi.umn.edu.
Young-In ChiThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. ychi@hi.umn.edu.
Jill SuttlesDepartment of Microbiology and Immunology, University of Louisville, 319 Abraham Flexner Way, Louisville, KY, 40202, USA. jill.suttles@louisville.edu.
Bing LiThe Hormel Institute, University of Minnesota, 801 16th Avenue, NE, Austin, MN, 55912, USA. bli@hi.umn.edu.
University of Minnesota · USUniversity of Louisville Hospital · US

Funding

Prevention of Breast Cancer Development by Epidermal Fatty Acid Binding Protein (R01CA180986 · NCI · UNIVERSITY OF MINNESOTA · PI LI, BING · 2014 to 2025
$3.3M
Fatty Acid Binding Proteins in Macrophage FunctionR01AI048850 · NIAID · UNIVERSITY OF LOUISVILLE · PI SUTTLES, JILL · 2003 to 2013
$3.2M
The role of adipocyte/macrophage fatty acid binding protein in breast cancer deveR01CA177679 · NCI · UNIVERSITY OF MINNESOTA · PI LI, BING · 2014 to 2018
$1.6M
NCI NIH HHS CA177679-01A1NCI NIH HHS R01 CA177679NCI NIH HHS R01 CA180986NCI NIH HHS R01-CA180986-01A1NIAID NIH HHS R01 AI048850NIAID NIH HHS R01-AI048850
6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) is an autoimmune disease in which dysregulated immune cells attack myelin in the central nervous system (CNS), leading to irreversible neuronal degeneration. Our previous studies have demonstrated that epidermal fatty acid binding protein (E-FABP), widely expressed in immune cells, in particular in dendritic cells (DCs) and T lymphocytes, fuels the overactive immune responses in the mouse model of experimental autoimmune encephalomyelitis (EAE).

methodsIn the present study, we conducted an intensive computational docking analysis to identify novel E-FABP inhibitors for regulation of immune cell functions and for treatment of EAE.

resultsWe demonstrate that compound [2-(4-acetylphenoxy)-9,10-dimethoxy-6,7-dihydropyrimido[6,1-a]isoquinolin-4-one; designated as EI-03] bound to the lipid binding pocket of E-FABP and enhanced the expression of peroxisome proliferator-activating receptor (PPAR) γ. Further in vitro experiments showed that EI-03 regulated DC functions by inhibition of TNFα production while promoting IL-10 secretion. Moreover, EI-03 treatment counterregulated T cell balance by decreasing effector T cell differentiation (e.g. Th17, Th1) while increasing regulatory T cell development. Most importantly, mice treated with this newly identified compound exhibited reduced clinical symptoms of EAE in mouse models.

conclusionsTaken together, we have identified a new compound which displays a potential therapeutic benefit for treatment of MS by targeting E-FABP.

Indexed as

Molecular Targeted TherapyAnimalsCell DifferentiationCytokinesDendritic CellsDrug Evaluation, PreclinicalEncephalomyelitis, Autoimmune, ExperimentalFatty Acid-Binding ProteinsMice, Inbred C57BLMolecular Docking SimulationNeoplasm ProteinsCytokinesFabp5 protein, mouseFatty Acid-Binding ProteinsNeoplasm Proteins

Identifiers

PMID25962726
PMCPMC4427938
OpenAlexW1841228419

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.