Evidence map›Paper›PMID 19692652›Full record

ArticleAmerican journal of physiology. Cell physiology2009

MEK, p38, and PI-3K mediate cross talk between EGFR and TNFR in enhancing hepatocyte growth factor production from human mesenchymal stem cells.

Yue Wang, Brent R Weil, Jeremy L Herrmann, Aaron M Abarbanell, Jiangning Tan, Troy A Markel, Megan L Kelly, Daniel R Meldrum

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2009. 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
1.9field-weighted citation impact, top 15% 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, 37 citations in OpenAlex.

  1. Understanding the role of TNFR2 signaling in the tumor microenvironment of breast cancer.Journal of experimental & clinical cancer research : CR · 2024
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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

8 authors at 1 institution in 2 countries.

Yue WangDepartments of Surgery, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Brent R Weil
Jeremy L Herrmann
Aaron M Abarbanell
Jiangning Tan
Troy A Markel
Megan L Kelly
Daniel R Meldrum
Indiana University – Purdue University Indianapolis · US

Funding

TNRF1 Signaling Resistance in Ischemic Human Female MyocardiumR01HL085595 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MELDRUM, DANIEL R · 2007 to 2010
$1.8M
Progenitor cell pretreatment against acute surgical I/RR01GM070628 · NIGMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MELDRUM, DANIEL R · 2004 to 2008
$1.5M
IL-18 Signaling in Mesenchymal Stem Cells: Function and Surgial ProtectionF32HL092718 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI ABARBANELL, AARON · 2008 to 2009
$103k
Neonatal Stem Cells: Unique Traits in Paracine Signaling and CardioprotectionF32HL092719 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI HERRMANN, JEREMY · 2008 to 2009
$101k
Sex differences in TNFR2 signaling mechanisms following acute surgical ischemiaF32HL093987 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI WEIL, BRENT RICHARD · 2009 to 2009
$50k
NHLBI NIH HHS F32 HL092718-01NHLBI NIH HHS F32 HL092719-01NHLBI NIH HHS F32 HL093987-01A1NHLBI NIH HHS K99/R00 HL0876077-01NHLBI NIH HHS R01HL085595NIGMS NIH HHS R01GM070628
6 · The paper itself

Abstract

Human bone marrow mesenchymal stem cells (MSCs) are a potent source of growth factors, which are partly responsible for their beneficial paracrine effects. We reported previously that transforming growth factor-alpha (TGF-alpha), a putative mediator of wound healing and the injury response, increases the release of vascular endothelial growth factor (VEGF), augments tumor necrosis factor-alpha (TNF-alpha)-stimulated VEGF production, and activates mitogen-activated protein kinases and phosphatidylinositol 3-kinase (PI-3K) pathway in human MSCs. The experiments described in this report indicate that TGF-alpha increases MSC-derived hepatocyte growth factor (HGF) production. TGF-alpha-stimulated HGF production was abolished by inhibition of MEK, p38, PI-3K, or by small interfering RNA (siRNA) targeting TNF receptor 2 (TNFR2), but was not attenuated by siRNA targeting TNF receptor 1 (TNFR1). Ablation of TNFR1 significantly increased basal and stimulated HGF. A potent synergy between TGF-alpha and TNF-alpha was noted in MSC HGF production. This synergistic effect was abolished by MEK, P38, PI-3K inhibition, or by ablation of both TNF receptors using siRNA. We conclude that 1) novel cross talk occurs between tumor necrosis factor receptor and TGF-alpha/epidermal growth factor receptor in stimulating MSC HGF production; 2) this cross talk is mediated, at least partially, via activation of MEK, p38, and PI-3K; 3) TGF-alpha stimulates MSCs to produce HGF by MEK, p38, PI-3K, and TNFR2-dependent mechanisms; and 4) TNFR1 acts to decrease basal TGF-alpha and TNF-alpha-stimulated HGF.

Indexed as

Blotting, WesternEnzyme-Linked Immunosorbent AssayErbB ReceptorsHepatocyte Growth FactorHumansMAP Kinase Kinase KinasesMesenchymal Stem Cellsp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptor Cross-TalkReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRNA, Small InterferingSignal TransductionTransforming Growth Factor alphaTumor Necrosis Factor-alphaErbB ReceptorsHepatocyte Growth FactorMAP Kinase Kinase Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRNA, Small InterferingTransforming Growth Factor alphaTumor Necrosis Factor-alpha

Identifiers

PMID19692652
PMCPMC2777403
OpenAlexW1994814948

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.