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Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency

ABSTRACT: Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency

PROVIDER: PRJNA1025271 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26318154.fastq.gz	Fastqsanger.gz
	SRR26318155.fastq.gz	Fastqsanger.gz

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Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-186]

Project description:Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-186]

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Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-237]

Project description:Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-237]

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Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency.

Project description:The resting zone of the postnatal growth plate is organized by slow-cycling chondrocytes expressing parathyroid hormone-related protein (PTHrP), which include a subgroup of skeletal stem cells that contribute to the formation of columnar chondrocytes. The PTHrP-Indian hedgehog feedback regulation is essential for sustaining growth plate activities; however, molecular mechanisms regulating cell fates of PTHrP+ resting chondrocytes and their eventual transformation into osteoblasts remain largely undefined. Here, in a mouse model, we specifically activated Hedgehog signaling in PTHrP+ resting chondrocytes and traced the fate of their descendants using a tamoxifen-inducible Pthrp-creER line with patched-1-floxed and tdTomato reporter alleles. Hedgehog-activated PTHrP+ chondrocytes formed large, concentric, clonally expanded cell populations within the resting zone ("patched roses") and generated significantly wider columns of chondrocytes, resulting in hyperplasia of the growth plate. Interestingly, Hedgehog-activated PTHrP+ cell descendants migrated away from the growth plate and transformed into trabecular osteoblasts in the diaphyseal marrow space in the long term. Therefore, Hedgehog activation drives resting zone chondrocytes into transit-amplifying states as proliferating chondrocytes and eventually converts these cells into osteoblasts, unraveling a potentially novel Hedgehog-mediated mechanism that facilitates osteogenic cell fates of PTHrP+ skeletal stem cells.

| S-EPMC10906233 | biostudies-literature

Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-11 | GSE244884 | GEO

Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-237]

Project description:A single cell transcriptional profile of growth plate cells of the murine femur at postnatal day 36 (P36), lineage-marked by PTHrP-creER at P6, Control

2023-10-11 | GSE244881 | GEO

Hedgehog activation promotes osteogenic fates of growth plate resting zone chondrocytes through transient clonal competency [NovaA-186]

Project description:A single cell transcriptional profile of growth plate cells of the murine femur at postnatal day 36 (P36), lineage-marked by PTHrP-creER at P6

2023-10-11 | GSE244880 | GEO

LMD-RNAseq of resting chondrocytes and proliferative chondrocytes

Project description:We investigated the molecular mechanisms that regulate the self-renewal and differentiation of chondroprogenitors by comparing the transcriptome profiles between resting chondrocytes and proliferative chondrocytes

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LMD-RNAseq of resting chondrocytes and proliferative chondrocytes

Project description:LMD-RNAseq of resting chondrocytes and proliferative chondrocytes

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Apolipoprotein E is a marker of all chondrocytes in the growth plate resting zone

Project description:The resting zone (RZ) in mammalian growth plates is critical for maintaining and regulating chondrocyte turnover during longitudinal bone growth as a control tower and stem cell reservoir. Although recent lineage tracing studies have identified several markers for stem cells in the RZ, these markers only partially label chondrocytes in the RZ, suggesting that the resting chondrocytes (RCs) are a heterogeneous population with different types of stem cells. Since a comprehensive marker for RCs is still lacking, the RZ is generally determined based on ambiguous histological criteria, such as small and round chondrocytes without columnar formation, which may lead to inconsistencies among researchers. Therefore, in this study, we used single-cell RNA sequencing (scRNAseq) of growth plate chondrocytes followed by validation by fluorescence in situ hybridization (FISH) to precisely annotate cell clusters in scRNAseq and search for a marker of RCs. The scRNAseq analysis revealed that apolipoprotein E (Apoe) was the top-hit gene, which was ubiquitously expressed in the RC cluster. FISH confirmed that Apoe was exclusively localized to the histologically defined RZ. In newly generated ApoemCherry knock-in mice, we further confirmed that mCherry expression mirrored the distribution of Apoe-expressing chondrocytes in the RZ particularly after the formation of the secondary ossification center. These mCherry+ RCs were slow cycling in vivo and exhibited stem cell properties in vitro. Moreover, APOE was detected in human growth plate RCs. These findings suggest that apolipoprotein E is a novel pan-RC marker in both mouse and human growth plates.

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SHP2 Regulates the Osteogenic Fate of Growth Plate Hypertrophic Chondrocytes.

Project description:Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been reported, yet the underlying molecular mechanism remains incompletely understood. SHP2 is an ubiquitously expressed cytoplasmic protein tyrosine phosphatase. SHP2 loss-of-function mutations in chondroid cells are linked to metachondromatosis in humans and mice, suggesting a crucial role for SHP2 in the skeleton. However, the specific role of SHP2 in skeletal cells has not been elucidated. To approach this question, we ablated SHP2 in collagen 2α1(Col2α1)-Cre- and collagen 10α1(Col10α1)-Cre-expressing cells, predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gene excision. Mice lacking SHP2 in Col2α1-Cre-expressing cells die at mid-gestation. Postnatal SHP2 ablation in the same cell population caused dwarfism, chondrodysplasia and exostoses. In contrast, mice in which SHP2 was ablated in the Col10α1-Cre-expressing cells appeared normal but were osteopenic. Further mechanistic studies revealed that SHP2 exerted its influence partly by regulating the abundance of SOX9 in chondrocytes. Elevated and sustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation to osteoblasts and impaired endochondral ossification. Our study uncovered an important role of SHP2 in bone development and cartilage homeostasis by influencing the osteogenic differentiation of hypertrophic chondrocytes and provided insight into the pathogenesis and potential treatment of skeletal diseases, such as osteopenia and osteoporosis.

| S-EPMC5629218 | biostudies-literature

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