| First Author | Bartolome F | Year | 2017 |
| Journal | J Neuroinflammation | Volume | 14 |
| Issue | 1 | Pages | 26 |
| PubMed ID | 28143489 | Mgi Jnum | J:317345 |
| Mgi Id | MGI:6850080 | Doi | 10.1186/s12974-017-0800-2 |
| Citation | Bartolome F, et al. (2017) Obesity and neuroinflammatory phenotype in mice lacking endothelial megalin. J Neuroinflammation 14(1):26 |
| abstractText | BACKGROUND: The multiligand receptor megalin controls the brain uptake of a number of ligands, including insulin and leptin. Despite the role of megalin in the transport of these metabolically relevant hormones, the role of megalin at the blood-brain-barrier (BBB) has not yet been explored in the context of metabolic regulation. METHODS: Here we investigate the role of brain endothelial megalin in energy metabolism and leptin signaling using an endothelial cell-specific megalin deficient (EMD) mouse model. RESULTS: We found megalin is important to protect mice from developing obesity and metabolic syndrome when mice are fed a normal chow diet. EMD mice developed neuroinflammation, by triggering several pro-inflammatory cytokines, displayed reduced neurogenesis and mitochondrial deregulation. CONCLUSIONS: These results implicate brain endothelial megalin expression in obesity-related metabolic changes through the leptin signaling pathway proposing a potential link between obesity and neurodegeneration. |
