A beta inhibits mesenchymal stem cell-pericyte transition through MAPK pathway

作者：Xu, Lixia; Li, Jialin; Luo, Zhongqiu; Wu, Qiaoli; Fan, Weijia; Yao, Xiuhua; Li, Qingguo^*; Yan, Hua^*; Wang, Jinhuan^*

来源：Acta Biochimica et Biophysica Sinica, 2018, 50(8): 776-781.

DOI：10.1093/abbs/gmy072

• Alzheimer's disease
• pericyte
• A beta
• MSC

Multiple independent reports have demonstrated pericyte loss in both the hippocampus and cortex in human Alzheimer's disease (AD). The differentiation and recruitment of pericytes are the essential steps in vasculature development. However, the role of amyloid beta (A beta) in pericyte differentiation has not yet been fully elucidated. In this study, we investigated the interaction between A beta and differentiation of mesenchymal stem cells (MSCs) toward pericytes in culture. Our results showed that mice overexpressing A beta-precursor protein (APP/PS1) exhibited the loss of pericytes compared with the control group mice, evidenced by the lack of desmin expression in the cortex of 12-month-old mice. Interestingly, we further found that both A beta(40) and A beta(42) inhibited the expressions of pericyte markers (alpha-SMA, desmin, and PDGFR beta) in cultured MSCs which can be differentiated into mature pericytes. Mechanistically, the inhibitory effects of A beta s on MSC-pericyte transition is mediated by the activation of the ERK1/2 MAPK signal pathway. These new insights into the roles of A beta in pericyte differentiation may help to develop more effective strategies for the treatment of AD.

• 出版日期2018-8
• 单位天津市环湖医院