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Partial ablation of osteocytes alters lineage cell specifications in bone and bone marrow, resulting in the acceleration of skeletal aging.

Profiling the adipocyte secretome reveals LRG1 as a novel adipokine that promotes insulin sensitivity and modulates inflammation triggered by release of cytochrome c from dead/dying cells, describing a new pathway at the intersection of obesity and its systemic sequelae.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.

Bone marrow adipocyte lipolysis is required for maintaining bone mass under conditions of energy deficiency and is necessary for myelopoiesis following caloric restriction and irradiation.

Non-imprinted genes can contribute to parent-of-origin effects on phenotype through interactions with imprinted genes.

A novel population of adipocytes that play essential roles in adaptive thermogenesis via cell autonomous and non-autonomous effects and regulate systemic glucose metabolism in mice.

Hypertrophic chondrocytes of the growth plate undergo a process of dedifferentiation to generate marrow associated skeletal stem and progenitor cells (SSPCs), which ultimately re-differentiate into cells of the osteoblast or adipocyte lineages during skeletal development.

A novel secondary adipogenesis pathway is defined that is unique to the bone marrow and is activated with age and in states of metabolic stress.

Adipsin, the oldest known adipokine, has a novel role as a a regulator of bone marrow fat and, consequently, overall bone health.

Murine periosteum is highly enriched for osteoprogenitors, many of which express αSMA, but fracture callus chondrocytes are partially derived from other sources.