| First Author | Liang C | Year | 2012 |
| Journal | Brain Res | Volume | 1455 |
| Pages | 103-13 | PubMed ID | 22510281 |
| Mgi Jnum | J:186457 | Mgi Id | MGI:5432332 |
| Doi | 10.1016/j.brainres.2011.10.051 | Citation | Liang C, et al. (2012) MicroRNA-153 negatively regulates the expression of amyloid precursor protein and amyloid precursor-like protein 2. Brain Res 1455:103-13 |
| abstractText | Increased expression of the amyloid precursor protein (APP) is a crucial risk factor of Alzheimer's disease (AD). Amyloid precursor-like protein 2 (APLP2), a homologue of APP, is also suggested to participate in AD pathogenesis. Accumulating evidence suggest the regulatory role of microRNA on AD-related genes. Here we showed that the levels of miR-153 were significantly decreased at early- and late-stage of AD in APPswe/PSDeltaE9 murine model. Moreover, a binding site of miR-153 on APP and APLP2-3'UTR was identified, respectively, by luciferase assay. Gain and loss of function experiments demonstrated that miR-153 suppressed the expression of APP and APLP2. Using miR-153 transgenic mouse model, we testified that miR-153 downregulated the expression of APP and APLP2 protein in vivo. Furthermore, closely related expression patterns of miR-153 and APP/APLP2 during brain development indicated a physiological regulation role of miR-153 on the two genes. In a neuronal cell line treated with Abeta(42) peptides and H(2)O(2,) the levels of miR-153 varied during time-course leading to corresponding changes of APLP2 protein, indicating Abeta peptides and oxidative stress influence the expression of miR-153. Thus, miR-153 contributes to post-transcriptional regulation of APP/APLP2, suggesting a possible role for miR-153 in neuro-pathological conditions. |
