Role for β1 integrins in cortical osteocytes during acute musculoskeletal disuse

The Matricellular Protein Periostin Is Required for Sost Inhibition and the Anabolic Response to Mechanical Loading and Physical Activity

“…Second, periostin activates the integrin signaling pathways (Akt/phosphatidylinositol 3-kinase) (42,43), which we also found in UMR-106 osteoblast-like cells (data not shown). Integrins are known to mediate osteocyte response to mechanical stimulation (44,45), and it is possible therefore that periostin contributes to Sost inhibition by co-activating integrin signaling in these cells. In addition, phosphatidylinositol 3-kinase/Akt signaling may influence Wnt-LRP5 signaling by inhibiting GSK3 kinase and releasing ␤-catenin from its inhibitory complex (46 -48).…”

CCAAT/enhancer binding protein β-deficiency enhances type 1 diabetic bone phenotype by increasing marrow adiposity and bone resorption

“…Mouse femurs were subjected to three-point bending to determine their mechanical properties (21,22,24,47,49). Specimens were thawed at room temperature prior to testing and kept wet in saline solution.…”

Role of Endocrine and Paracrine Factors in the Adaptation of Bone to Mechanical Loading

“…Our experiments have shown that mechanical strain sensitizes the osteoblastic response to endogenous IGF-1 levels [17••], which would suggest that risk factors for osteoporosis capable of reducing basal IGF-1 levels could well attenuate the IGF-1 component of the adaptive response. It has also recently been shown that β 1 integrin, which is required for loading-related bone formation in vivo [36] as well as bone loss caused by disuse [37], can be regulated by ERα and that this is a mechanism by which estrogen can augment the expression of target genes [38].…”