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  Mesenchymal stem cells attenuate inflammatory processes in the heart and lung via inhibition of TNF signaling

Martire, A., Bedada, F. B., Uchida, S., Poeling, J., Krüger, M., Warnecke, H., et al. (2016). Mesenchymal stem cells attenuate inflammatory processes in the heart and lung via inhibition of TNF signaling. BASIC RESEARCH IN CARDIOLOGY, 111(5): 54. doi:10.1007/s00395-016-0573-2.

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 Creators:
Martire, Alessandra1, Author           
Bedada, Fikru B.1, Author           
Uchida, Shizuka1, Author           
Poeling, Jochen1, Author           
Krüger, Marcus1, Author           
Warnecke, Henning, Author
Richter, Manfred, Author
Kubin, Thomas1, Author           
Herold, Susanne, Author
Braun, Thomas1, Author           
Affiliations:
1Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591698              

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Free keywords: TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE-CELLS; BONE-MARROW; STROMAL CELLS; FAILURE; THERAPY; ETANERCEPT; ACTIVATION; MECHANISMS; EXPRESSIONCardiovascular System & Cardiology; Mesenchymal stem cells; Proteomics; TNF-alpha; Fibrosis; Inflammation; Heart failure; Acute lung injury;
 Abstract: Mesenchymal stem cells ( MSC) have been used to treat different clinical conditions although the mechanisms by which pathogenetic processes are affected are still poorly understood. We have previously analyzed the homing of bone marrow-derived MSC to diseased tissues characterized by a high degree of mononuclear cell infiltration and postulated that MSC might modulate inflammatory responses. Here, we demonstrate that MSC mitigate adverse tissue remodeling, improve organ function, and extend lifespan in a mouse model of inflammatory dilative cardiomyopathy ( DCM). Furthermore, MSC attenuate Lipopolysaccharide-induced acute lung injury indicating a general role in the suppression of inflammatory processes. We found that MSC released sTNF-RI, which suppressed activation of the NFjBp65 pathway in cardiomyocytes during DCM in vivo. Substitution of MSC by recombinant soluble TNF-R partially recapitulated the beneficial effects of MSC while knockdown of TNF-R prevented MSC-mediated suppression of the NFjBp65 pathway and improvement of tissue pathology. We conclude that sTNF-RI is a major part of the paracrine machinery by which MSC effect local inflammatory reactions.

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Language(s): eng - English
 Dates: 2016
 Publication Status: Published online
 Pages: 13
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: ISI: 000382683900002
DOI: 10.1007/s00395-016-0573-2
 Degree: -

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Title: BASIC RESEARCH IN CARDIOLOGY
Source Genre: Journal
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Publ. Info: TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY : SPRINGER HEIDELBERG
Pages: - Volume / Issue: 111 (5) Sequence Number: 54 Start / End Page: - Identifier: ISSN: 0300-8428