Modulating endothelial adhesion and migration impacts stem cell therapies efficacy.

Background: Limited knowledge of stem cell therapies` mechanisms of action hampers their sustainable implementation into the clinic. Specifically, the interactions of transplanted stem cells with the host vasculature and its implications for their therapeutic efficacy are not elucidated. We tested whether adhesion receptors and chemokine receptors on stem cells can be functionally modulated, and consequently if such modulation may substantially affect therapeutically relevant stem cell interactions with the host endothelium.

PK11195, a specific ligand of the peripheral benzodiazepine receptor, may protect pancreatic beta-cells from cytokine-induced cell death.

We cultured isolated islets from human or porcine origin in the presence or absence of IL1 and TNFα and studied cytoprotective effects of two structurally different PBR ligands. Storage of pig or human islets in the presence of cytokines significantly lowered the fraction of vital beta-cells. Compared with cytokine incubations PK11195 alone or in combination with cytokines was effective to prevent cytokine induced cell death.

Expression of blood group genes by mesenchymal stem cells.

Incompatible blood group antigens are highly immunogenic and can cause graft rejections. Focusing on distinct carbohydrate- and protein-based membrane structures, defined by blood group antigens, we investigated human bone marrow-derived mesenchymal stem cells (MSCs) cultured in human serum. The presence of H (CD173), ABO, RhD, RhCE, RhAG, Kell, urea transporter type B (SLC14A1, previously known as JK), and Duffy antigen receptor of chemokines (DARC) was evaluated at the levels of genome, transcriptome and antigen.