دورية أكاديمية
Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling
| العنوان: | Cord Blood Mesenchymal Stromal Cell-Conditioned Medium Protects Endothelial Cells via STAT3 Signaling |
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| المؤلفون: | Bader, Andreas Matthaeus, Brodarac, Andreja, Klose, Kristin, Bieback, Karen, Choi, Yeong-Hoon, Kang, Kyung-Sun, Kurtz, Andreas, Stamm, Christof |
| المساهمون: | Kang, Kyung-Sun, Kurtz, Andreas |
| بيانات النشر: | S. Karger AG |
| سنة النشر: | 2020 |
| المجموعة: | Seoul National University: S-Space |
| مصطلحات موضوعية: | CRITICAL LIMB ISCHEMIA, STEM-CELLS, IN-VITRO, BONE-MARROW, MYOCARDIAL-INFARCTION, PARACRINE MECHANISMS, PROMOTE ANGIOGENESIS, HYPOXIA, APOPTOSIS, TRANSPLANTATION, Cell therapy, Endothelial cell, Ischemia, Stem cell, Cord blood |
| الوصف: | Background/Aims: Cell-based therapies may be useful for treating ischemic diseases, but the underlying mechanisms are incompletely understood. We investigated the impact of cord blood mesenchymal stromal cell (CBMSC)- or fibroblast (FB)-secreted factors on starved endothelial cells and determined the relevant intracellular signaling pathways. Methods: HUVECs were subjected to glucose/serum deprivation (GSD) in hypoxia or normoxia, in presence of CBMSC- or FB-conditioned medium (CM). Viability and proliferation were determined via WST-8 conversion and BrdU incorporation. Apoptosis was quantified by annexin V/ethidium homodimer-III staining, nuclear fragmentation and cell morphology. mRNA expression and protein phosphorylation were determined by real-time qPCR and western blot. Experiments were repeated in presence of small molecule inhibitors. Results: The negative impact of GSD was most pronounced at 21% O-2. Here, medium of CBMSCs and FBs increased viability and proliferation and reduced apoptosis of HUVECs. This was associated with increased STAT3 and ERK1/2 phosphorylation and BCL-2 expression. Under STAT3 inhibition, the beneficial effect of CBMSC-CM on viability and BCL-2 expression was abolished. Conclusion: Factors released by CBMSCs protect endothelial cells from the deleterious impact of GSD by activation of the STAT3 survival pathway. However, this phenomenon is not CBMSC-specific and can be reproduced using juvenile fibroblasts. Copyright (C) 2014 S. Karger AG, Basel ; Y ; 1 |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| تدمد: | 1015-8987 |
| العلاقة: | Cellular Physiology and Biochemistry, Vol.34 No.3, pp.646-657; https://hdl.handle.net/10371/192309Test; 000343765200004; 2-s2.0-84906609891; 106606 |
| DOI: | 10.1159/000363030 |
| الإتاحة: | https://doi.org/10.1159/000363030Test https://hdl.handle.net/10371/192309Test |
| رقم الانضمام: | edsbas.950A24F2 |
| قاعدة البيانات: | BASE |
| تدمد: | 10158987 |
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| DOI: | 10.1159/000363030 |