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Full spectrum flow cytometry reveals a high degree of placental mesenchymal cell heterogeneity, which is lost with culture, highlighting the importance of detailed ex vivo phenotyping to optimise the use of these cells in downstream applications.

Cytomegaloviruses are recognized by distinct sensors depending on the infected cell type and together these sensors are essential for viral control and downstream immune responses.

A unique functional comparison of the major endometrial cell types from 44 control and endometriosis patients demonstrates not only a uterine origin of the disease, but also that endometrial to mesothelial cell gap junctions are required for invasive lesion formation.

Single-cell RNA sequencing of neonatal uterus revealed an Misr2+ endometrial stromal progenitor whose inhibition by ectopic administration of MIS caused uterine hypoplasia and infertility in adulthood.

Experimentation on patient biopsies, cell culture, and xenograft models demonstrates involvement of ErbB signaling and fibroblasts in lesion growth, implying that targeting of both stromal and endothelial cells could be a beneficial treatment strategy for patients with venous lesions.

Metformin selectively improves bone healing of three types of bone injuries in hyperglycemic but not in normoglycemic mice.

Blastocyst complementation of rat embryos with donor mouse embryonic stem cells was used to simultaneously produce multiple, donor-derived hematopoietic and stromal cells in the interspecies bone marrow that exhibited normal gene expression signatures, cell surface markers, and functional characteristics.

Comprehensive scRNA-seq analysis of cardiac stromal cells in healthy and injured hearts reveals novel cell types and non-linear cell dynamics, providing new insights into cardiac inflammation, fibrosis and repair.

Developing long bones contain distinct mesenchymal stem-cell populations derived from mesoderm and neural crest, which have specialized functions in skeleton formation and the establishment of the hematopoietic stem-cell niche, respectively.

Mouse models reveal fundamental roles of SMAD1/5 in mediating both bone morphogenetic protein signaling pathways and the transcriptional response to progesterone during decidualization.