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The stanniocalcin-1-dependent immunosuppressive roles of mesenchymal stem cell on chimeric antigen receptor modified T cell therapy.

Age-stratified comparisons of gene expression in progeria patient fibroblasts reveals disruption of mesenchymal lineage pathways and points to a deficit in chondrogenic commitment in early development and a depletion of the mesenchymal lineage stem cell pool.

Single-cell sequencing of the alveolar bone marrow of apical periodontitis reveals the cellular and molecular composition of the microenvironment and highlights an osteogenic potential within mesenchymal stem cells of inflammatory-related bone diseases.

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.

Bone formation in adult mice can be induced by a bone-binding, recombinant version of the Notch ligand Delta-like 4 without triggering adverse effects in other organs.

Senescent cells accumulate in the fracture callus and a reduction in the number of these cells accelerates fracture healing in mice.

Fibro-adipogenic progenitors in skeletal muscle contribute to the neuromuscular pathogenesis of spinal muscular atrophy, and depletion of SMN in chondrocytes reduces local IGF sigaling in growth plate.

The inhibition of colorectal cancer (CRC) proliferation, migration, and invasion is attributed to BEST4, which exhibits epistasis over Hes4 in the downregulation of Twist1 and consequent suppression of epithelial-to-mesenchymal transition in CRC.

Bone cells exposed to physiological forces release ATP through repairable membrane injury, generating an intercellular signal that conveys the destructive potential of forces and the adaptive capacity of endangered cells.