Journal
JOURNAL OF IMMUNOLOGY RESEARCH
Volume 2015, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2015/183738
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Funding
- Chinese National Natural Science Foundation [81172841, 81202368, 81471603]
- China Postdoctoral Science Foundation [2013M541708]
- Natural Science Foundation of Jiangsu Colleges and Universities Grant [09KJB320010]
- project of Jiangsu Provincial Health Department [Z201005]
- innovative project of Nantong University postgraduate students [13025043]
- Jiangsu Province's Outstanding Medical Academic Leader Program [LJ201136]
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Previous studies indicated that bone marrow mesenchymal stem cells (BM-MSCs) from patients with systemic lupus erythematosus (SLE) exhibited the phenomenon of apoptosis. In this study, we aimed to investigate whether apoptosis of BM-MSCs from SLE patients were dysregulated. In this paper, endoplasmic reticulum stress (ERS) was evidenced by increased expression of phosphorylated protein kinase RNA-like ER kinase (PERK) and inositol-requiring protein-1 (IRE-1). We also found the activation of downstream target eukaryotic translation initiator factor 2 alpha (eIF 2 alpha) and CCAAT/enhancer-binding protein-(C/EBP-) homologous protein (CHOP) in BM-MSCs from SLE patients. Interestingly, we discovered that 4-phenylbutyric acid (4-PBA), a selective inhibitor of ERS, blocked the apoptosis of BM-MSCs from SLE patients and alleviated the level of Jun N-terminal kinase1/2 (JNK1/2) and CHOP. Furthermore, blockage of PERK signaling expression by siRNA not only significantly reduced the expression of CHOP, but also activated the anti-apoptotic regulator B-cell lymphoma-2 (Bcl-2). Blockage of IRE-1 or JNK1/2 by siRNA resulted in the decreased expression of JNK1/2 and proapoptosis protein Bcl-2 associated protein X (BAX). These results implicated that ERS-mediated apoptosis was a critical determinant of BM-MSCs from SLE patients.
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