Gli1 labels progenitors during chondrogenesis in postnatal mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1050820 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27167547_1.fastq.gz | Fastqsanger.gz | |||
| SRR27167547_2.fastq.gz | Fastqsanger.gz | |||
| SRR27167548_1.fastq.gz | Fastqsanger.gz | |||
| SRR27167548_2.fastq.gz | Fastqsanger.gz | |||
| SRR27167549_1.fastq.gz | Fastqsanger.gz |
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Project description:Skeletal growth promoted by endochondral ossification is tightly coordinated by self-renewal and differentiation of chondrogenic progenitors. Emerging evidence has shown that multiple skeletal stem cells (SSCs) participate in cartilage formation. However, as yet, no study has reported the existence of common long-lasting chondrogenic progenitors in various types of cartilage. Here, we identified Gli1+ chondrogenic progenitors (Gli1+ CPs), which were distinct from SSCs, were responsible for the lifelong generation of chondrocytes in the growth plate, vertebrae, ribs, and other cartilage. The absence of Gli1+ CPs led to cartilage defects and dwarfishness phenotype in mice. Furthermore, we found that the BMP signal played an important role in self-renewal and maintenance of Gli1+ CPs. The deletion of Bmpr1α caused the exhaustion of Gli1+ CPs, consequently disrupting columnar cartilage. Collectively, our data demonstrate that Gli1+ CPs are common long-term chondrogenic progenitors in multiple types of cartilage and are essential to maintain cartilage homeostasis.
2024-02-18 | GSE249831 | GEO
Project description:Skeletal growth promoted by endochondral ossification is tightly coordinated by self-renewal and differentiation of chondrogenic progenitors. Emerging evidence has shown that multiple skeletal stem cells (SSCs) participate in cartilage formation. However, as yet, no study has reported the existence of common long-lasting chondrogenic progenitors in various types of cartilage. Here, we identify Gli1+ chondrogenic progenitors (Gli1+ CPs), which are distinct from PTHrP+ or FoxA2+ SSCs, are responsible for the lifelong generation of chondrocytes in the growth plate, vertebrae, ribs, and other cartilage. The absence of Gli1+ CPs leads to cartilage defects and dwarfishness phenotype in mice. Furthermore, we show that the BMP signal plays an important role in self-renewal and maintenance of Gli1+ CPs. Deletion of Bmpr1α triggers Gli1+ CPs quiescence exit and causes the exhaustion of Gli1+ CPs, consequently disrupting columnar cartilage. Collectively, our data demonstrate that Gli1+ CPs are common long-term chondrogenic progenitors in multiple types of cartilage and are essential to maintain cartilage homeostasis.
| S-SCDT-10_1038-S44319-024-00093-X | biostudies-other
Project description:Skeletal growth promoted by endochondral ossification is tightly coordinated by self-renewal and differentiation of chondrogenic progenitors. Emerging evidence has shown that multiple skeletal stem cells (SSCs) participate in cartilage formation. However, as yet, no study has reported the existence of common long-lasting chondrogenic progenitors in various types of cartilage. Here, we identify Gli1+ chondrogenic progenitors (Gli1+ CPs), which are distinct from PTHrP+ or FoxA2+ SSCs, are responsible for the lifelong generation of chondrocytes in the growth plate, vertebrae, ribs, and other cartilage. The absence of Gli1+ CPs leads to cartilage defects and dwarfishness phenotype in mice. Furthermore, we show that the BMP signal plays an important role in self-renewal and maintenance of Gli1+ CPs. Deletion of Bmpr1α triggers Gli1+ CPs quiescence exit and causes the exhaustion of Gli1+ CPs, consequently disrupting columnar cartilage. Collectively, our data demonstrate that Gli1+ CPs are common long-term chondrogenic progenitors in multiple types of cartilage and are essential to maintain cartilage homeostasis.
| S-EPMC11014955 | biostudies-literature
Project description:The goal of this study is to investigate the role of Gli1+ osteogenic progenitors in the development of TMJOA.
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Project description:Gli1+ progenitors are considered as metaphyseal mesenchymal progenitors in the distal femur and proximal tibia under the growth plate. We used single cell RNA sequencing (scRNA-seq) to analyze the diversity of Gli1+ progenitors in response to methylprednisolone.
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Project description:Inhibiting Hh signaling in Gli1+ osteogenic progenitors alleviates TMJOA
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Project description:The morphogen and mitogen, Sonic Hedgehog, activates a Gli1-dependent transcription program that drives proliferation of granule neuron progenitors (GNPs) within the external germinal layer of the postnatally developing cerebellum. Medulloblastomas with mutations activating the Sonic Hedgehog signaling pathway preferentially arise within the external germinal layer, and the tumor cells closely resemble GNPs. Atoh1/Math1, a basic helix-loop-helix transcription factor essential for GNP histogenesis, does not induce medulloblastomas when expressed in primary mouse GNPs that are explanted from the early postnatal cerebellum and transplanted back into the brains of naïve mice. However, enforced expression of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost three orders of magnitude. Unlike Gli1, Atoh1 cannot support GNP proliferation in the absence of Sonic Hedgehog signaling and does not govern expression of canonical cell cycle genes. Instead, Atoh1 maintains GNPs in a Sonic Hedgehog-responsive state by regulating genes that trigger neuronal differentiation, including many expressed in response to bone morphogenic protein-4. Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development. Keywords: disease state analysis 14 samples, 1 time series, 2 engineered Medulloblastoma tumors
2010-07-08 | E-GEOD-19684 | biostudies-arrayexpress
Project description:Teriparatide, a bioactive fragment of human parathyroid hormone (PTH), is the most widely prescribed bone anabolic drug in the world, but its cellular targets remain incompletely defined. The Gli1+ metaphyseal mesenchymal progenitors (MMPs) are a main source for osteoblasts in postnatal growing mice, but their potential response to teriparatide is unknown. Here, by lineage tracing we find that teriparatide stimulates both proliferation and osteoblast differentiation of MMPs. Single-cell RNA sequencing reveals heterogeneity among MMPs including a chondrocyte-like osteoprogenitor (herein COP) population that expands in response to teriparatide. COPs express the highest level of Hedgehog (Hh) target genes and the insulin-like growth factor receptor Igf1r. Inhibition of Hh signaling, or selective deletion of Igf1r in MMPs diminishes the proliferative and osteogenic effects of teriparatide. The study therefore identifies MMPs as teriparatide target cells wherein Hh and Igf signaling are critical for osteoblast production.
2021-06-06 | GSE169560 | GEO
Project description:In order to characterize mRNA expression in the growth plate, we microdissected postnatal rat growth plates into their constituent zones and used microarray analysis to assess the abundences of individual transcripts. Expression patterns of PTHrP and Ihh-related genes were confirmed using real-time PCR. Using a gli1-lacZ mouse, Gli1 expression, presumably representing Ihh signaling, was visualized during pre- and postnatal development. Microdissection was used to collect individual growth plate zones from proximal tibiae of 1-wk rats and gene expression was analyzed using microarray.
2010-12-01 | E-GEOD-23432 | biostudies-arrayexpress
Project description:The morphogen and mitogen, Sonic Hedgehog, activates a Gli1-dependent transcription program that drives proliferation of granule neuron progenitors (GNPs) within the external germinal layer of the postnatally developing cerebellum. Medulloblastomas with mutations activating the Sonic Hedgehog signaling pathway preferentially arise within the external germinal layer, and the tumor cells closely resemble GNPs. Atoh1/Math1, a basic helix-loop-helix transcription factor essential for GNP histogenesis, does not induce medulloblastomas when expressed in primary mouse GNPs that are explanted from the early postnatal cerebellum and transplanted back into the brains of naïve mice. However, enforced expression of Atoh1 in primary GNPs enhances the oncogenicity of cells overexpressing Gli1 by almost three orders of magnitude. Unlike Gli1, Atoh1 cannot support GNP proliferation in the absence of Sonic Hedgehog signaling and does not govern expression of canonical cell cycle genes. Instead, Atoh1 maintains GNPs in a Sonic Hedgehog-responsive state by regulating genes that trigger neuronal differentiation, including many expressed in response to bone morphogenic protein-4. Therefore, by targeting multiple genes regulating the differentiation state of GNPs, Atoh1 collaborates with the pro-proliferative Gli1-dependent transcriptional program to influence medulloblastoma development. Keywords: disease state analysis
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