Evidence map›Paper›PMID 24569592›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2014

Regulation of hepatocyte growth factor expression by NF-κB and PPARγ in adipose tissue.

Jun Yin, Jong Han Lee, Jin Zhang, Zhanguo Gao, Vsevolod Y Polotsky, Jianping Ye

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Hypoxia-induced alternative splicing: the 11th Hallmark of Cancer.Journal of experimental & clinical cancer research : CR · 2020
    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

6 authors at 4 institutions in 2 countries.

Jun YinPennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana;
Jong Han Lee
Jin Zhang
Zhanguo Gao
Vsevolod Y Polotsky
Jianping Ye
Louisiana State University System · USJohns Hopkins Medicine · USPennington Biomedical Research Center · USShanghai Jiao Tong University · CN

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2005 to 2026
$26.5M
THE ROLE OF PROTEIN MALNUTRITION ON CIRCADIAN PHYSIOLOGY OF C57BL/6J MOUSE DAMSP20RR021945 · NCRR · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI GETTYS, THOMAS W · 2006 to 2011
$9.5M
Mechanism of IKK in FFA-associated Insulin ResistanceR01DK068036 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI YE, JIANPING · 2004 to 2013
$2.7M
Adipose Tissue Hypoxia and Inflammation in ObesityR01DK085495 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI YE, JIANPING · 2010 to 2013
$1.3M
Regulation of Energy Expenditure by NF-kBR56DK068036 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI YE, JIANPING · 2009 to 2015
$296k
NCRR NIH HHS 2P20-RR-021945NIDDK NIH HHS 2P30-DK-072476NIDDK NIH HHS DK-085495NIDDK NIH HHS DK-68036NIDDK NIH HHS P30 DK072476
6 · The paper itself

Abstract

Hepatocyte growth factor (HGF) is expressed as an angiogenic factor in adipose tissue. However, the molecular mechanism of Hgf expression remains largely unknown in the tissue. We addressed the issue by studying Hgf expression in adipocytes and macrophages. Hgf was expressed more in the stromal-vascular fraction than the adipocyte fraction. The expression was fivefold more in macrophages than the stromal-vascular faction and was reduced by 50% after macrophage deletion in adipose tissue. The expression was reduced by differentiation in adipocytes and by tumor necrosis factor-α or lipopolysaccharide treatment in macrophages. The expression was suppressed by nuclear factor (NF)-κB in C57BL/6 mice with NF-κB p65 overexpression under the aP2 gene promoter (aP2-p65 mice) but enhanced by inactivation of NF-κB p65 in mouse embryonic fibroblasts. The Hgf gene promoter was suppressed by p65 overexpression, which blocked peroxisome proliferator-activated receptor-γ (PPARγ) interaction with RNA polymerase II. The p65 activity was abolished by knockdown of histone deacetylase 3. Hgf expression was upregulated by hypoxia in vitro and in vivo. Compared with vascular endothelial growth factor (Vegf), which was predominately expressed in mature adipocytes, Hgf was mainly expressed in nonadipocytes, suggesting that Hgf and Vegf may have different cell sources in adipose tissue. In mechanism, Hgf expression is inhibited by NF-κB through suppression of PPARγ function in the Hgf gene promoter. Both Hgf and Vegf are induced by hypoxia. The study provides a molecular mechanism for the difference of inflammation and hypoxia in the regulation of angiogenic factors.

Indexed as

3T3-L1 CellsAdipose TissueAnimalsCells, CulturedGene Expression RegulationHEK293 CellsHepatocyte Growth FactorHumansMaleMiceMice, Inbred C57BLMice, ObeseMice, TransgenicNIH 3T3 CellsPPAR gammaTranscription Factor RelAHepatocyte Growth FactorPPAR gammaRela protein, mouseTranscription Factor RelAadipose tissue hypoxiainflammationmacrophage infiltrationmice with nuclear factor-κB p65 overexpression under the Ap2 gene promoternuclear factor-κBperoxisome proliferator-activated receptor-γvascular endothelial growth factor

Identifiers

PMID24569592
PMCPMC3989740
OpenAlexW2055260898

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.