Osteocyte apoptosis is required for production of osteoclastogenic signals following bone fatigue in vivo.

摘要: Osteocyte apoptosis is spatially, temporally and functionally linked to the removal replacement of microdamage in bone. Recently we showed that elicits distinct responses two populations osteocytes near injury site. Osteocytes directly adjacent undergo apoptosis, whereas there a second group located apoptotic population upregulate expression osteoclastogenic signaling molecules. In this study used pan-caspase inhibitor QVD test hypothesis osteocyte an obligatory step production key signals by situ fatigue-damaged We found, based on real-time PCR immunohistochemistry assays, marker caspase-3 as well proteins RANKL VEGF were increased following fatigue, while antagonist OPG decreased. However, when was inhibited using QVD, these changes gene completely blocked. This dependence for neighboring non-apoptotic cells produce promote tissue remodeling also occurs response focal ischemic brain heart, indicating osteoclastic bone follows common paradigm localized repair.