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Human Bone Marrow Derived Mesenchymal Stem Cells Regulate Leukocyte-Endothelial Interactions and Activation of Transcription Factor NF-Kappa B | OMICS International | Abstract
ISSN: 2157-7552

Journal of Tissue Science & Engineering
Open Access

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Research Article

Human Bone Marrow Derived Mesenchymal Stem Cells Regulate Leukocyte-Endothelial Interactions and Activation of Transcription Factor NF-Kappa B

Phillip A. Letourneau1,2, Tyler D. Menge1, Kathryn A. Wataha1, Charles E. Wade1,2, Charles S.Cox Jr3, John B. Holcomb1,2 and Shibani Pati1,2*
1Center for Translational Injury Research, Texas Medical School at Houston, Houston, TX, USA
2Department of Surgery, Texas Medical School at Houston, Houston, TX, USA
3Department of Pediatric Surgery, Texas Medical School at Houston, Houston, TX, USA
Corresponding Author : Shibani Pati, MD, PhD
Assistant Professor for Translational Injury Research
Department of Surgery University of Texas School of Medicine
Houston 6431 Fannin St. MSB 5.212 Houston, TX 77030
Tel: 713-500-5417
Fax: 713-512-7135
E-mail: [email protected]
Received July 06, 2011; Accepted July 23, 2011; Published July 25, 2011
Citation: Letourneau PA, Menge TD, Wataha KA, Wade CE, Cox CS Jr, et al. (2011) Human Bone Marrow Derived Mesenchymal Stem Cells Regulate Leukocyte-Endothelial Interactions and Activation of Transcription Factor NFKappa B. J Tissue Sci Eng S3:001. doi: 10.4172/2157-7552.S3-001
Copyright: © 2011 Letourneau PA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Bone marrow derived mesenchymal stem cells (MSCs) have been shown to demonstrate benefit in multiple disease models characterized by inflammation such as sepsis and acute lung injury. Mechanistically we hypothesized that MSCs exhibit these properties through inhibition of leukocyte activation and modulation of leukocyte-endothelial interactions; key interlinked processes involved in the deleterious effects of injury and inflammation. In this paper we found that MSCs co-cultured with a monocytoid line, U937, inhibit U937 binding to pulmonary endothelial cells (PECs) stimulated with the inflammatory cytokine TNF?. Furthermore, we show that these effects on functional adhesion are not due to changes in inflammatory adhesion molecule expression on U937s. No changes were found in CD62L, CD29, CD11b and CD18 expression on U937s co-cultured with MSCs. To determine if the effects of MSCs on leukocyte-endothelial interactions are due to the effects of MSCs on leukocyte activation, we investigated whether MSCs affect functional activation of the transcription factor NF-Kappa B. We found that MSCs significantly inhibit transcriptional activation of NF-kappa B in U937s. We also found that MSCs inhibit DNA binding of NF-kappa B subunits p50 and p65 to putative NF-kappa B DNA binding sites. Concomitant with a decrease in NF-kappa B activation was a significant increase in IL-10, an anti-inflammatory cytokine known to inhibit activation of NF-kappa B. Taken together, these findings show that MSCs have potent effects on leukocyte-endothelial interactions which may be due to the direct effects of MSCs on IL-10 and NF-kB. These findings suggest a potential therapeutic role for MSCs in diseases characterized by inflammation such as acute lung injury or multi-organ failure induced by traumatic injury.

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