| First Author | Xu L | Year | 2018 |
| Journal | Acta Biochim Biophys Sin (Shanghai) | Volume | 50 |
| Issue | 8 | Pages | 776-781 |
| PubMed ID | 29939221 | Mgi Jnum | J:351921 |
| Mgi Id | MGI:7703872 | Doi | 10.1093/abbs/gmy072 |
| Citation | Xu L, et al. (2018) Abeta inhibits mesenchymal stem cell-pericyte transition through MAPK pathway. Acta Biochim Biophys Sin (Shanghai) 50(8):776-781 |
| abstractText | 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 (Abeta) in pericyte differentiation has not yet been fully elucidated. In this study, we investigated the interaction between Abeta and differentiation of mesenchymal stem cells (MSCs) toward pericytes in culture. Our results showed that mice overexpressing Abeta-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 Abeta40 and Abeta42 inhibited the expressions of pericyte markers (alpha-SMA, desmin, and PDGFRbeta) in cultured MSCs which can be differentiated into mature pericytes. Mechanistically, the inhibitory effects of Abetas on MSC-pericyte transition is mediated by the activation of the ERK1/2 MAPK signal pathway. These new insights into the roles of Abeta in pericyte differentiation may help to develop more effective strategies for the treatment of AD. |
