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    Mesenchymal stem cells protect islets from hypoxia/reoxygenation-induced injury

    Access Status
    Fulltext not available
    Authors
    Lu, Y.
    Jin, X.
    Chen, Younan
    Li, S.
    Yuan, Y.
    Mai, G.
    Tian, B.
    Long, D.
    Zhang, J.
    Zeng, L.
    Li, Y.
    Cheng, J.
    Date
    2010
    Type
    Journal Article
    
    Metadata
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    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.
    Source Title
    Cell Biochemistry and Function
    DOI
    10.1002/cbf.1701
    ISSN
    0263-6484
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/3539
    Collection
    • Curtin Research Publications
    Abstract

    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.

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