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Stem Cells International
Volume 2017, Article ID 7316354, 13 pages
Research Article

Kindlin-2 Modulates the Survival, Differentiation, and Migration of Induced Pluripotent Cell-Derived Mesenchymal Stromal Cells

1Department of Transfusion Medicine, Cell Therapeutics and Hemostaseology, Ludwig-Maximilians University Hospital, Munich, Germany
2Translational Hepatology and Stem Cell Biology, REBIRTH Cluster of Excellence and Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany
3Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Münster, Germany
4Blood Transfusion Service, SRC, Zürich, Switzerland
5Blood Transfusion Service, SRC, Chur, Switzerland

Correspondence should be addressed to Reinhard Henschler; ed.xmg@relhcsnehr

Received 23 September 2016; Revised 24 November 2016; Accepted 12 December 2016; Published 9 January 2017

Academic Editor: Andrea Ballini

Copyright © 2017 Mohsen Moslem et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Kindlin-2 is a multidomain intracellular protein that can be recruited to β-integrin domains to activate signaling, initiate transcriptional programs, and bind to E-cadherin. To explore its involvement in cell fate decisions in mesenchymal cells, we studied the effects of Kindlin-2 modification (overexpression/knockdown) in induced pluripotent cell-derived mesenchymal stromal cells (iPSC-MSCs). Kindlin-2 overexpression resulted in increased proliferation and reduced apoptosis of iPSC-MSCs, as well as inhibition of their differentiation towards osteocytes, adipocytes, and chondrocytes. In contrast, siRNA-mediated Kindlin-2 knockdown induced increased apoptosis and increased differentiation response in iPSC-MSCs. The ability of iPSC-MSCs to adhere to VCAM-1/SDF-1α under shear stress and to migrate in a wound scratch assay was significantly increased after Kindlin-2 overexpression. In contrast, inhibition of mixed lymphocyte reaction (MLR) was generally independent of Kindlin-2 modulation in iPSC-MSCs, except for decreased production of interleukin-2 (IL-2) after Kindlin-2 overexpression in iPS-MSCs. Thus, Kindlin-2 upregulates survival, proliferation, stemness, and migration potential in iPSC-MSCs and may therefore be beneficial in optimizing performance of iPSC-MSC in therapies.