Mesenchymal stem cells protect islets from hypoxia/reoxygenation-induced injury
|dc.identifier.citation||Lu, Y. and Jin, X. and Chen, Y. and Li, S. and Yuan, Y. and Mai, G. and Tian, B. et al. 2010. Mesenchymal stem cells protect islets from hypoxia/reoxygenation-induced injury. Cell Biochemistry and Function. 28 (8): pp. 637-643.|
Hypoxia/reoxygenation (H/R)-induced injury is the key factor associated with islet graft dysfunction. This study aims to examine the effect of mesenchymal stem cells (MSCs) on islet survival and insulin secretion under H/R conditions. Islets from rats were isolated, purified, cultured with or without MSCs, and exposed to hypoxia (O2 = 1%) for 8 h and reoxygenation for 24 and 48 h, respectively. Islet function was evaluated by measuring basal and glucose-stimulated insulin secretion (GSIS). Apoptotic islet cells were quantified using Annexin V-FITC. Anti-apoptotic effects were confirmed by mRNA expression analysis of hypoxia-resistant molecules, HIF-1a, HO-1, and COX-2, using semi-quantitative retrieval polymerase chain reaction (RT-PCR). Insulin expression in the implanted islets was detected by immunohistological analysis. The main results show that the stimulation index (SI) of GSIS was maintained at higher levels in islets co-cultured with MSCs. The MSCs protected the islets from H/R-induced injury by decreasing the apoptotic cell ratio and increasing HIF-1a, HO-1, and COX-2 mRNA expression. Seven days after islet transplantation, insulin expression in the MSC-islets group significantly differed from that of the islets-alone group. We proposed that MSCs could promote anti-apoptotic gene expression by enhancing their resistance to H/R-induced apoptosis and dysfunction. This study provides an experimental basis for therapeutic strategies based on enhancing islet function. © 2010 John Wiley & Sons, Ltd.
|dc.title||Mesenchymal stem cells protect islets from hypoxia/reoxygenation-induced injury|
|dcterms.source.title||Cell Biochemistry and Function|
|curtin.department||School of Biomedical Sciences|
|curtin.accessStatus||Fulltext not available|
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