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Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE228319 | GEO | 2026/03/09

REPOSITORIES: GEO

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Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

Project description:Single cell RNA-sequencing was performed to examine the transcriptomic identity of RANKL-expressing cells during fracture healing in mice. RANKL fate-mapping mice were used to isolate tdTomato-labeled cells from tibiae at post-fracture day 14.

2026-03-09 | GSE315785 | GEO

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [scRNA-seq]

Project description:Single-cell RNA-sequencing was performed to examine the transcriptional landscape of murine fetal primary ossification center in early bone and bone marrow development. We particularly focused on the identification of potential osteoclast-inducing cells in the developing bone and aimed to analyzed its cellular fates.

2026-03-09 | GSE228318 | GEO

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [bulk RNA-seq]

Project description:RNA-sequencing was performed to examine the transcriptional characteristics of cells involved in osteoclast induction in murine fetal bone.

2026-03-09 | GSE228317 | GEO

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

Project description:Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

| PRJNA949250 | ENA

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

Project description:Medullary cavity expansion is mediated by distinct cell populations during fetal bone development

| PRJNA1399162 | ENA

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [scRNA-seq]

Project description:Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [scRNA-seq]

| PRJNA949255 | ENA

Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [bulk RNA-seq]

Project description:Medullary cavity expansion is mediated by distinct cell populations during fetal bone development [bulk RNA-seq]

| PRJNA949253 | ENA

NOTCH1 signaling establishes the medullary thymic epithelial cell progenitor pool during mouse fetal development.

Project description:The cortical and medullary thymic epithelial cell (cTEC and mTEC) lineages are essential for inducing T cell lineage commitment, T cell positive selection and the establishment of self-tolerance, but the mechanisms controlling their fetal specification and differentiation are poorly understood. Here, we show that notch signaling is required to specify and expand the mTEC lineage. Notch1 is expressed by and active in TEC progenitors. Deletion of Notch1 in TECs resulted in depletion of mTEC progenitors and dramatic reductions in mTECs during fetal stages, consistent with defects in mTEC specification and progenitor expansion. Conversely, forced notch signaling in all TECs resulted in widespread expression of mTEC progenitor markers and profound defects in TEC differentiation. In addition, lineage-tracing analysis indicated that all mTECs have a history of receiving a notch signal, consistent with notch signaling occurring in mTEC progenitors. These data provide strong evidence for a requirement for notch signaling in specification of the mTEC lineage.

| S-EPMC7328004 | biostudies-literature

Inhibited Maternal Bone Resorption Suppress Fetal Rat Bone Development During Pregnancy.

Project description:Objective:To determine the relationship between maternal bone resorption and bone development in fetuses. Methods:Female SD rats were injected with either fluorescent calcium indicator calcein alone or together with tetracycline 1 week before pregnancy, followed by fluorescence detection in fetal tibias 21 days post-treatment. Alendronate was subsequently administered to pregnant rats to inhibit maternal bone resorption, while maternal bone turnover and fetal bone development were both examined. Results:The maternal fluorescent labeled calcium before pregnancy was found in the fetal tibia. This indicated that the calcium of maternal bones may be released into the maternal circulation through high bone resorption during pregnancy, thereby participating in the fetal bone development. Bone histomorphometry and serum biomarker results showed that Alendronate significantly inhibited maternal bone resorption in pregnant rats when compared to normal pregnant rats. Moreover, the body weight, bone mass, and bone length of the fetuses in the Alendronate group were significantly decreased; while no apparent abnormality in placental morphology was observed. The above results implied that when maternal bone resorption is suppressed, the development of the fetal bone shall also be suppressed. Conclusion:Calcium in the maternal bone is released into the maternal circulation through bone resorption during pregnancy which represents an important material source in fetal bone development. Therefore, high bone turnover during pregnancy is essential for mammalian embryonic bone development.

| S-EPMC7042177 | biostudies-literature

The transcriptional cofactor Lbh regulates angiogenesis and endochondral bone formation during fetal bone development.

Project description:Lbh is thought to act as a transcriptional cofactor and is highly conserved among species. Here we show that Lbh is expressed in chondrocytes, cells of the perichondrium, and the primary spongiosa in fetal growth plates of mice and chickens. Lbh overexpression in chick wings, using the RCAS-retroviral vector strategy, results in shortened skeletal elements and delayed hypertrophic chondrocyte maturation and bone formation. Additionally, osteoclast and endothelial cell invasion are delayed in the Lbh-overexpressing bones. Finally, we find a dramatic suppression of Runx2 and VEGF mRNAs in chondrocytes and osteoblasts that overexpress Lbh. Strikingly, this abnormal bone development in infected limbs can be rescued by concurrent overexpression of Runx2. These results suggest that during endochondral bone formation, Lbh may negatively regulate vascular invasion and formation of the early ossification center at least in part by interfering with Runx2 and/or VEGF expression.

| S-EPMC2760734 | biostudies-literature

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