Moreover, omentin-1 preconditioning for 1 h could protect MSCs against H 2O 2-induced apoptosis in a concentration-dependent manner. Results After treatment with omentin-1 (100–800 ng/ml), MSCs displayed a higher proliferative capacity with an increasing number of cells in the S and G2 phase of the cell cycle. The cytokine secretion was assessed by ELISA. Tube formation assay was used to test the angiogenesis role of conditioned medium from MSCs in vitro. Expression levels of Akt, FoxO3a, GSK-3β, and apoptosis- and cell cycle-associated proteins were detected by Western blotting. Hoechst 33342 dye was used to assess morphological changes of apoptosis. Cell cycle, apoptosis ratio, reactive oxygen species concentration, and mitochondrial membrane potential were detected by flow cytometry. Cell proliferation was assessed with CCK-8 and EdU assay. Methods MSCs were isolated from 60–80 g donor rats.
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Click the above file 'GPPROEX312000D1.exe' to download the file to the desired folder. Remarkably, PI3K/Akt-related signaling pathways are known to function as core mechanisms by regulating multiple cellular behaviors of MSCs such as proliferation, survival, proangiogenesis, cytokine production, and so on. Unfortunately, the insufficient numbers of such MSCs obtained from donors, the low survival in the harsh environment, and the poor function of donor cells has limited their therapeutic potential. Background Mesenchymal stem cells (MSCs) are adult stem cells and have attracted great interest for cell-based therapeutic strategies for tissue injury, such as myocardial infarction, stroke, and hind limb ischemia, because of their easy preparation, immunologic privilege, and ethical advantage. Furthermore, omentin-1 enhanced Akt phosphorylation however, blockade of the PI3K/Akt pathway with an inhibitor, (20 μM), suppressed the above beneficial effects of omentin-1. Omentin-1 could enhance angiogenic growth factor secretion and elevate the ability of MSCs to stimulate tube formation by human umbilical vein endothelial cells (HUVECs). Western blots revealed that increased Bcl-2 and decreased Bax appeared in MSCs after omentin-1 incubation, which inhibited the mitochondrial apoptosis pathways with evidence showing inhibition of caspase-3 cleavage and preservation of mitochondrial membrane potential.
Furthermore, omentin-1 pretreatment reduced the excessive reactive oxygen species. 3.0 Limited Edition is now available! Needs registration.
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