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STAT3 mediates bone marrow mesenchymal stem cell VEGF production.

STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Research Abstract Details 

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  • STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Abstract Text:

    meijing wangMeijing Wang,wenjun zhangWenjun Zhang,paul crisostomoPaul Crisostomo,troy markelTroy Markel,kirstan k meldrumKirstan K Meldrum,xin y fuXin Y Fu,daniel r meldrumDaniel R Meldrum,

    The mechanisms by which mesenchymal stem cells (MSCs) may protect native tissue are incompletely understood. Understanding the mechanisms by which these cells release factors such as vascular endothelial growth factor (VEGF), may lead to enhanced protection. We hypothesized that stress, in the form of hypoxia or TNF, activates MSCs to release VEGF by STAT3 and p38 MAPK dependent mechanisms. Mouse MSCs from wild type (WT) and STAT3 knockout mice (STAT3KO) were harvested and purified by a single-step method using adhesion. The release of VEGF was analyzed by using MSC conditioned media under hypoxia or TNF stimulation with or without p38 MAPK inhibition. Activation of STAT3 and p38 MAPK was determined by analysis of cell lysates. MSCs released VEGF under normoxia, which was associated with constitutive STAT3 activity. STAT3 deficiency resulted in decreased MSC production of VEGF. In response to hypoxia or TNF, MSCs produced more VEGF, which was correlated with hypoxia or TNF activated p38 MAPK and STAT3. The p38 MAPK inhibitor significantly decreased hypoxia-induced or TNF-stimulated VEGF production in WT. Additionally, STAT3 ablation neutralized hypoxia-induced MSC release of VEGF. No effect of p38 MAPK inhibitor alone was observed on MSC release of VEGF in WT. However, inhibition of p38 MAPK blocked release of VEGF in STAT3KO MSCs. MSCs are a potent source of VEGF, the production of which is mediated by STAT3 under normoxia partly; however, following hypoxia or TNF exposure, MSC release of VEGF is mediated by both STAT3 and p38 MAPK.

    STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Publishing Authors By Initials

    m wangM Wang,w zhangW Zhang,p crisostomoP Crisostomo,t markelT Markel,kk meldrumKK Meldrum,xy fuXY Fu,dr meldrumDR Meldrum,

    For similar peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research abstracts see: peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research

    PUBMED ID PMID:

    MEDLINE DATE:

    STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of molecular and cellular cardiology

    VOLUME: 42

    Page Numbers: 1009-15

    Journal Abbreviation: J. Mol. Cell. Cardiol.

    ISSN: 0022-2828

    DAY: 24

    MONTH: 04

    YEAR: 2007

    STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 262322

    STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Keywords Mesh Terms:

    KEYWORDS: Vascular Endothelial Growth Factor A

    MESH TERMS: biosynthesis

    Chemical & Substance for Abstract: STAT3 mediates bone marrow mesenchymal stem cell VEGF production. Information

    Substance Name: Vascular Endothelial Growth Factor A

    Registry Number: 0

    Grant and Affiliation Information for STAT3 mediates bone marrow mesenchymal stem cell VEGF production.

    AFFILIATION: Department of Surgery, Indiana University School of Medicine, Indianapolis, IN 46202, USA.

    Country: England

    England Research PublicationEngland Research Publication

    AGENCY: United States NIGMS

    GRANT: R01 GM 070628

    ACRONYM: GM

    MEDLINETA: J Mol Cell Cardiol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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