MTORC1 Signaling is a Critical Regulator of Postnatal Tendon Development.
Ontology highlight
ABSTRACT: Tendons transmit contractile forces between musculoskeletal tissues. Whereas the biomechanical properties of tendons have been studied extensively, the molecular mechanisms regulating postnatal tendon development are not well understood. Here we examine the role of mTORC1 signaling in postnatal tendon development using mouse genetic approaches. Loss of mTORC1 signaling by removal of Raptor in tendons caused severe tendon defects postnatally, including decreased tendon thickness, indicating that mTORC1 is necessary for postnatal tendon development. By contrast, activation of mTORC1 signaling in tendons increased tendon cell numbers and proliferation. In addition, Tsc1 conditional knockout mice presented severely disorganized collagen fibers and neovascularization in the tendon midsubstance.
SUBMITTER: Lim J
PROVIDER: S-EPMC5719403 | biostudies-literature | 2017 Dec
REPOSITORIES: biostudies-literature
ACCESS DATA