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Lgr5-expressing secretory cells form a Wnt inhibitory niche in cartilage critical for chondrocyte identity

ABSTRACT: Lgr5-expressing secretory cells form a Wnt inhibitory niche in cartilage critical for chondrocyte identity

PROVIDER: PRJNA993104 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25213288_1.fastq.gz	Fastqsanger.gz
	SRR25213288_2.fastq.gz	Fastqsanger.gz
	SRR25213289_1.fastq.gz	Fastqsanger.gz
	SRR25213289_2.fastq.gz	Fastqsanger.gz
	SRR25213290_1.fastq.gz	Fastqsanger.gz

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Lgr5-expressing secretory cells form a Wnt inhibitory niche in cartilage critical for chondrocyte identity

Project description:We performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage cells from post-traumatic temporomandibular joint osteoarthritis model to investigate the signaling pathways critical for cellular functions during temporomandibular joint osteoarthritis pathology.

2023-07-13 | GSE236909 | GEO

Lgr5-expressing secretory cells form a Wnt inhibitory niche in cartilage critical for chondrocyte identity.

Project description:Osteoarthritis is a degenerative joint disease that causes pain, degradation, and dysfunction. Excessive canonical Wnt signaling in osteoarthritis contributes to chondrocyte phenotypic instability and loss of cartilage homeostasis; however, the regulatory niche is unknown. Using the temporomandibular joint as a model in multiple species, we identify Lgr5-expressing secretory cells as forming a Wnt inhibitory niche that instruct Wnt-inactive chondroprogenitors to form the nascent synovial joint and regulate chondrocyte lineage and identity. Lgr5 ablation or suppression during joint development, aging, or osteoarthritis results in depletion of Wnt-inactive chondroprogenitors and a surge of Wnt-activated, phenotypically unstable chondrocytes with osteoblast-like properties. We recapitulate the cartilage niche and create StemJEL, an injectable hydrogel therapy combining hyaluronic acid and sclerostin. Local delivery of StemJEL to post-traumatic osteoarthritic jaw and knee joints in rabbit, rat, and mini-pig models restores cartilage homeostasis, chondrocyte identity, and joint function. We provide proof of principal that StemJEL preserves the chondrocyte niche and alleviates osteoarthritis.

| S-EPMC10790417 | biostudies-literature

The transient chondrocyte phenotype in osteophytic cartilage - a role of PEDF?

Project description:Pigment Epithelium-Derived Factor (PEDF) has recently been identified as a factor that is significantly upregulated in late-stage osteoarthritic cartilage in which chondrocytes are confronted with terminal differentiation and cell death. Since PEDF is known to induce cell death of endothelial cells, it may also be responsible for terminal differentiation and cell death in cartilage. Using cDNA microarray analysis, we found PEDF among the factors with the strongest differential expression and significant higher levels (118.5-fold) in osteophytic cartilage compared with articular cartilage. This study explored if PEDF interferes with the stable chondrocyte phenotype by promoting terminal differentiation or cell death.

2013-01-31 | E-GEOD-43923 | biostudies-arrayexpress

TRIM15 drives chondrocyte senescence and osteoarthritis progression

Project description:Chondrocyte senescence underlies osteoarthritis (OA). However, the pathogenesis of chondrocyte senescence remains largely unclear. Here we report that TRIM15 is a critical regulator in chondrocyte senescence. TIRM15 is highly expressed in chondrocytes of senescent cartilage from human OA patients and aged mice. Using gain- and loss-of-function studies, we further identify that TRIM15 facilitates chondrocyte senescence. Notably, conditional deletion of TRIM15 in chondrocytes severely impairs skeletal growth, partially due to the fact that embryonic chondrocyte senescence is disturbed. Compared with Col2a1-CreERT2/TRIM15flox/flox mice, TRIM15flox/flox mice exhibits accelerated OA phenotype, increased senescence markers and senescence-associated secretory phenotype (SASP) during aging. Mechanistically, TRIM15 binds with YAP and directly mediates K48-linked YAP ubiquitination at K254, which interrupts the interaction between YAP and AMOT, leading to enhanced YAP nuclear translocation. Intra-articular injection of AAV5-Trim15 shRNA decelerates OA progression in mice. Collectively, these findings indicate that targeting TRIM15 reshapes aging cartilage microenvironment and protects against OA.

2025-02-24 | GSE281609 | GEO

Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome

Project description:Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome

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Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run92]

Project description:The isolation of chondrocytes from human articular cartilage for single-cell RNA sequencing requires extensive and prolonged tissue digestion at 37 °C. Modulations of the transcriptional activity likely take place during this period such that the transcriptomes of isolated human chondrocytes no longer match their original status in vivo. Here, we optimized the human chondrocyte isolation procedure to maximally preserve the in vivo transcriptome.

2022-11-15 | GSE217870 | GEO

Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run54]

2022-11-15 | GSE217869 | GEO

Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run54]

Project description:Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run54]

| PRJNA901160 | ENA

Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run92]

Project description:Optimization of chondrocyte isolation from human articular cartilage to preserve the chondrocyte transcriptome [run92]

| PRJNA901161 | ENA

Reg4+ Deep Crypt Secretory cells function as epithelial niche for Lgr5+ stem cells in colon

Project description:Lgr5+ stem cells reside at crypt bottoms of the small and large intestine. Small intestinal Paneth cells supply Wnt3, EGF and Notch signals to neighboring Lgr5+ stem cells. While the colon lacks Paneth cells, Deep Crypt Secretory (DCS) cells are intermingled with Lgr5+ stem cells at crypt bottoms. Here, we report Reg4 as a marker of DCS cells. To investigate a niche function, we eliminated DCS cells using the diphtheria-toxin receptor gene knocked into the murine Reg4 locus. Ablation of DCS cells results in loss of stem cells from colonic crypts and disrupts gut homeostasis and colon mini-gut formation. In agreement, sorted Reg4+ DCS cells promote organoid formation of single Lgr5+ colon stem cells. Stem cells are forced to generate DCS cells in vitro by combined Notch inhibition and Wnt activation. We conclude that Reg4+ DCS cells serve as Paneth cell equivalents in the colon crypt niche.

2016-10-05 | GSE63256 | GEO

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