Umbilical cord blood mesenchymal stem cells protect amyloid-β42 neurotoxicity via paracrine.
Umbilical cord blood mesenchymal stem cells protect amyloid-β42 neurotoxicity via paracrine.
复制标题
脐带血间充质干细胞通过旁分泌保护淀粉样蛋白-β42 神经毒性。
作者：
Ju;Dong Hyun Kim;J. Kim;Yoon;W. Oh;E. Lee;J. Chang
目标
目的：探讨人脐血间充质干细胞对淀粉样蛋白42(Aβ42，Aβ42)损伤大鼠原代神经元的神经保护机制。
方法
为评价人脐血间充质干细胞对神经细胞的保护作用，将人脐血间充质干细胞与Aβ42暴露的大鼠原代神经细胞在Transwell仪中进行共培养。为了评估人脐血间充质干细胞释放的可溶性因子在神经保护中的作用，我们进行了基于抗体的共培养阵列。在共培养系统中，通过处理重组蛋白或针对每个候选蛋白的特定小干扰RNA(SiRNAs)来评估鉴定的hUCB-MSC蛋白的神经保护作用。
结果
当人脐血间充质干细胞与暴露于Aβ42的大鼠原代神经细胞共同培养时，其分泌的核心蛋白和原颗粒水平升高。重组核心蛋白聚糖和原颗粒蛋白对Aβ42神经毒性的保护作用此外，siRNA介导的hUCB-MSCs中核心蛋白聚糖和原颗粒蛋白的表达下调，降低了hUCB-MSC在共培养体系中的抗凋亡作用。
结论
核心蛋白聚糖和原颗粒蛋白可能参与了Aβ42诱导的人脐血间充质干细胞的抗凋亡活性。
AIM
To understand the neuroprotective mechanism of human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) against amyloid-β42 (Aβ42) exposed rat primary neurons.
METHODS
To evaluate the neuroprotective effect of hUCB-MSCs, the cells were co-cultured with Aβ42-exposed rat primary neuronal cells in a Transwell apparatus. To assess the involvement of soluble factors released from hUCB-MSCs in neuroprotection, an antibody-based array using co-cultured media was conducted. The neuroprotective roles of the identified hUCB-MSC proteins was assessed by treating recombinant proteins or specific small interfering RNAs (siRNAs) for each candidate protein in a co-culture system.
RESULTS
The hUCB-MSCs secreted elevated levels of decorin and progranulin when co-cultured with rat primary neuronal cells exposed to Aβ42. Treatment with recombinant decorin and progranulin protected from Aβ42-neurotoxicity in vitro. In addition, siRNA-mediated knock-down of decorin and progranulin production in hUCB-MSCs reduced the anti-apoptotic effects of hUCB-MSC in the co-culture system.
CONCLUSION
Decorin and progranulin may be involved in anti-apoptotic activity of hUCB-MSCs exposed to Aβ42.
影响因子：
23.9
作者：
Ranganath, Sudhir H.;Levy, Oren;Inamdar, Maneesha S.;Karp, Jeffrey M.
通讯作者：
Karp, Jeffrey M.
影响因子：
6.6
作者：
Schönherr, E;O'Connell, BC;Kresse, H
通讯作者：
Kresse, H