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人脐带血间充质干细胞分泌的半乳糖凝集素-3减少体外淀粉样β42 神经毒性。

Galectin-3 secreted by human umbilical cord blood-derived mesenchymal stem cells reduces amyloid-beta42 neurotoxicity in vitro.

机构信息

Biomedical Research Institute, MEDIPOST Co., Ltd., Seoul 137-874, Republic of Korea.

出版信息

FEBS Lett. 2010 Aug 20;584(16):3601-8. doi: 10.1016/j.febslet.2010.07.028. Epub 2010 Jul 24.

Abstract

In this study, we found that expression and secretion of galectin-3 (GAL-3) were upregulated by amyloid-beta42 (Abeta42) exposure in human umbilical cord blood-derived mesenchymal stem cell (hUCB-MSC) without cell death. Abeta42-exposed rat primary cortical neuronal cells co-treated with recombinant GAL-3 were protected from neuronal death in a dose-dependent manner. hUCB-MSCs were cocultured with Abeta42-exposed rat primary neuronal cells or the neuroblastoma cell line, SH-SY5Y in a Transwell chamber. Coculture of hUCB-MSCs reduced cell death of Abeta42-exposed neurons and SH-SY5Y cells. This neuroprotective effect of hUCB-MSCs was reduced significantly by GAL-3 siRNA. These data suggested that hUCB-MSC-derived GAL-3 is a survival factor against Abeta42 neurotoxicity.

摘要

在这项研究中,我们发现β淀粉样蛋白 42(Abeta42)暴露于人脐带血间充质干细胞(hUCB-MSC)中会导致半乳糖凝集素 3(GAL-3)的表达和分泌上调,而不会导致细胞死亡。Abeta42 暴露的大鼠原代皮质神经元细胞与重组 GAL-3 共同处理,以剂量依赖性方式防止神经元死亡。hUCB-MSCs 与 Abeta42 暴露的大鼠原代神经元细胞或神经母细胞瘤细胞系 SH-SY5Y 在 Transwell 室中共培养。hUCB-MSCs 与 Abeta42 暴露的神经元和 SH-SY5Y 细胞共培养可减少细胞死亡。hUCB-MSC 衍生的 GAL-3 通过 GAL-3 siRNA 显著降低了这种神经保护作用。这些数据表明,hUCB-MSC 衍生的 GAL-3 是对抗 Abeta42 神经毒性的存活因子。

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