APP promotes osteoblast survival and bone formation by regulating mitochondrial function and preventing oxidative stress.

ABSTRACT: Amyloid precursor protein (APP) is ubiquitously expressed in various types of cells including bone cells. Mutations in App gene result in early-onset Alzheimer's disease (AD). However, little is known about its physiological function in bone homeostasis. Here, we provide evidence for APP's role in promoting bone formation. Mice that knocked out App gene (APP^-/-) exhibit osteoporotic-like deficit, including reduced trabecular and cortical bone mass. Such a deficit is likely due in large to a decrease in osteoblast (OB)-mediated bone formation, as little change in bone resorption was detected in the mutant mice. Further mechanical studies of APP^-/- OBs showed an impairment in mitochondrial function, accompanied with increased reactive oxygen species (ROS) and apoptosis.

SUBMITTER: Pan JX 

PROVIDER: S-EPMC6197195 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature