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A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [scRNA-seq]

ABSTRACT: A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [scRNA-seq]

PROVIDER: PRJNA1133674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29754944_1.fastq.gz	Fastqsanger.gz
	SRR29754944_2.fastq.gz	Fastqsanger.gz
	SRR29754945_1.fastq.gz	Fastqsanger.gz
	SRR29754945_2.fastq.gz	Fastqsanger.gz
	SRR29754946_1.fastq.gz	Fastqsanger.gz

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A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [scRNA-seq]

Project description:Directed differentiation of stem cells toward chondrogenesis in vitro and in situ to regenerate cartilage suffers from off-target differentiation and hypertrophic tendency. Here, we generated a cartilaginous organoid system from human expanded pluripotent stem cells (hEPSCs) carrying a COL2A1mCherry and COL10A1eGFP double reporter, enabling real-time monitoring of chondrogenesis and hypertrophy. After screening 2,040 FDA-approved drugs, we found that α-adrenergic receptor (α-AR) antagonists, especially phentolamine, stimulated chondrogenesis but repressed hypertrophy, while α2-AR agonists reduced chondrogenesis and induced hypertrophy. Phentolamine prevented cartilage degeneration in hEPSC cartilaginous organoid and human cartilage explant models and stimulated microfracture-activated endogenous skeletal stem cells toward hyaline-like cartilage regeneration without fibrotic degeneration in situ. Mechanistically, α2-AR signaling induced hypertrophic degeneration via cyclic guanosine monophosphate (cGMP)-dependent secretory leukocyte protease inhibitor (SLPI) production. SLPI-deleted cartilaginous organoid was degeneration resistant, facilitating large cartilage defect healing. Ultimately, targeting α2-AR/SLPI was a promising and clinically feasible strategy to regenerate cartilage via promoting chondrogenesis and repressing hypertrophy.

2024-09-30 | GSE271814 | GEO

A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [bulk RNA-seq]

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A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration

Project description:A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration

| PRJNA1133672 | ENA

A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [bulk RNA-seq]

Project description:A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration [bulk RNA-seq]

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A human organoid drug screen identifies α2-adrenergic receptor signaling as a therapeutic target for cartilage regeneration

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

2024-09-30 | GSE271815 | GEO

Engraftment of allogeneic iPS cell-derived cartilage organoid in a primate model of articular cartilage defect

Project description:Engraftment of allogeneic iPS cell-derived cartilage organoid in a primate model of articular cartilage defect

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Engraftment of allogeneic iPS cell-derived cartilage organoid in a primate model of articular cartilage defect

Project description:Induced pluripotent stem cells (iPSCs) are a promising resource for allogeneic cartilage transplantation to treat articular cartilage defects that do not heal spontaneously and often progress to debilitating conditions, such as osteoarthritis. However, to the best of our knowledge, allogeneic cartilage transplantation into primate models has never been assessed. Here, we show that allogeneic iPSC-derived cartilage organoids survive and integrate as well as function as articular cartilage in a primate model of chondral defects in the knee joints. Histological analysis revealed that allogeneic iPSC-derived cartilage organoids in chondral defects elicited no immune reaction and directly contributed to the tissue repair for at least four months. iPSC-derived cartilage organoids integrated with the host native articular cartilage and prevented degeneration of the surrounding cartilage. Single-cell RNA-sequence analysis indicated that iPSC-derived cartilage organoids differentiated after transplantation, acquiring expression of PRG4 that is crucial for joint lubrication. Pathway analysis suggested the involvement of SIK3 inactivation, verified through molecular experiments. Our study outcomes suggest that allogeneic transplantation of iPSC-derived cartilage organoids may be clinically applicable for the treatment of patients with chondral defects of the articular cartilage.

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