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A hybrid mouse/human model using mesenchymal progenitor cells reveals dynamics of human adipose tissue development and mechanisms that may enhance human adipose thermogenic capacity.

Single-cell RNA-sequencing, spatial genomics, and histological analyses reveal that cold-induced brown adipose neogenesis is a complex adaptive response to elevated metabolic demand involving dynamic interactions between recruited immune cells and a subpopulation of poised adipocyte progenitors.

Single-cell transcriptomic profiling of human bone marrow non-hematopoietic cells provides the basis for a comprehensive understanding of the cellular complexity of the hematopoietic stem cell (HSC) microenvironment and the intricate stroma-hematopoiesis crosstalk mechanisms.

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

A group of cells that can become adipocytes controls the formation of blood vessels in the bone marrow, and also regulates the differentiation of resident mesenchymal progenitor cells.

Fibro-inflammatory progenitors represent a subpopulation of perivascular cells in visceral adipose tissues of mice that promote inflammation and fibrosis.

Combined fate mapping and genetic deletion studies reveal that PDGFRα+ cells and PDGFRα gene itself are required for adipose tissue development but not for adult tissue homeostasis.

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.

OGT-mediated protein O-GlcNAcylation balances osteogenic versus adipogenic differentiation and controls hematopoietic niche function of bone marrow stromal cells.