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ctt-journal > Aizenstadt A.2 et al. (Abstract)

Aizenstadt A.2 et al. (Abstract)

Cellular Therapy and Transplantation (CTT), Vol. 3, No. 12
doi: 10.3205/ctt-2011-No12-abstract81

© The Authors. This abstract is provided under the following license: Creative Commons Attribution 3.0 Unported

Abstract accepted for "5th Raisa Gorbacheva Memorial Meeting Hematopoietic Stem Cell Transplantation in Children and Adults", Saint Petersburg, Russia, September 18–20, 2011

Preliminary Program

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ICAM-1 content alteration on the cord blood mesenchymal stem cell's surface in response to the actions of proinflammatory cytokines

Alexandra A. Aizenstadt1, Vladimir B. Klimovich2, Alexander B. Smolyaninov1

1"Stem cell bank Pokrovsky", St. Petersburg, Russia; 2Russian Scientific Center for Radiology and Surgical Technologies, St. Petersburg, Russia

Correspondence: Alexander B. Smolyaninov, "Stem Cell Bank Pokrovsky", Bolshoi Prospect Vasilevski Ostrov 85, St. Petersburg, 199106, Russia, E-mail: stemcellbank@spam is badinbox.ru


Umbilical cord blood mesenchymal stem cells (CB MSC) are currently promising candidates for cell therapy of autoimmune diseases and GvHD. However, the mechanisms of their immunosuppressive influence have not been fully explained. Thus, there is no consensus around the question whether direct contact of MSC and immune system cells is required for immunosuppression, or whether the action of soluble factors is sufficient. At the same time, it has been shown that MSCs actively express ICAM-1 and VCAM-1, better showing immunosuppressive properties.

The purpose of this study was to determine whether the pro-inflammatory cytokines (particularly TNF-α and INF-γ, as well as C3a) influence ICAM-1 expression in the CB MSC.
Methods: MSCs were obtained from CB samples and cultured over up to 4 passages. Measurement of ICAM-1 levels was performed by flow cytometry with staining monoclonal antibodies against ICAM-1 conjugated with FITC.

Results: INF-γ (10 ng/ml) did not affect the expression of ICAM-1, but the effects of TNF-α (10 ng/ml) resulted in a significant increase of ICAM-1 on the surface of MSCs. Increased expression of ICAM-1 occurred in response to C3A (10 nM) to a lesser extent.

To find out, through which signaling pathway an increase in ICAM-1 occurs in response to TNF-α before the addition of a cytokine, over 1h cells were under the influence of inhibitors of signaling pathways, mediated by p38 MAPK (inhibitor SB203580), NFκB (QNZ), JNK 1/2/3 (SP600125), and MEK 1/2 (UO126). Reduction of ICAM-1 did not occur under the action of any of the above inhibitors, or in the case of all four at once.

Thus, TNF-α has most powerful influence on the content of ICAM-1 on the surface of the CB MSC among the analyzed cytokines, and this reaction is achieved through different signaling pathways than p38 MAPK, NFκB, JNK 1/2/3 and MEK 1/2.

Keywords: cord blood mesenchymal stem cells, ICAM-1, TNF-α