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Gene expression profile at single cell level of articular cartilage superficial cells from pulse and trace labeled tdTomato+ cells from Procr-CreER;tdTomato mice.

ABSTRACT: Characteristics of the chondroprogenitors cells remain unidentified. Here we identified a chondroprogenitor population, which specifically expresses Procr, and used single cell RNA sequencing (scRNA-seq) to analyze the diversity and differentiation of Procr-lineage cells in articular cartilage.

ORGANISM(S): Mus musculus

PROVIDER: GSE295257 | GEO | 2025/06/12

REPOSITORIES: GEO

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Gene expression profile at single cell level of articular cartilage superficial cells from sham and dmm surgery mice and long bone periosteum cells from steady state mice.

Project description:Characteristics of the chondroprogenitors cells remain unidentified. Here we identify a chondroprogenitor population, which specifically expresses Procr,and used single cell RNA sequencing (scRNA-seq) and bulk RNA-seq to analyze the diversity of Prcor+ cells in articular cartilage and periosteum.

2025-06-12 | GSE278533 | GEO

Gene expression profile at single cell level of articular cartilage superficial cells from pulse and trace labeled tdTomato+ cells from Procr-CreER tdTomato mice.

Project description:Gene expression profile at single cell level of articular cartilage superficial cells from pulse and trace labeled tdTomato+ cells from Procr-CreER tdTomato mice.

| PRJNA1253968 | ENA

Compensatory growth and recovery of tissue cytoarchitecture after transient cartilage-specific cell death in foetal mouse limbs

Project description:A major question in developmental and regenerative biology is how organ size is controlled by progenitor cells. For example, while limb bones exhibit catch-up growth (recovery of a normal growth trajectory after transient developmental perturbation), it is unclear how this emerges from the behaviour of chondroprogenitors, the cells sustaining the cartilage anlagen that are progressively replaced by bone. Here we show that transient sparse cell death in the mouse foetal cartilage was repaired postnatally, via a two-step process. During injury, progression of chondroprogenitors towards more differentiated states was delayed, leading to altered cartilage cytoarchitecture and impaired bone growth. Then, once cell death was over, chondroprogenitor differentiation was accelerated and cartilage structure recovered, including partial rescue of bone growth. At the molecular level, ectopic activation of mTORC1 correlated with, and was necessary for, part of the recovery, revealing a specific candidate to be explored during normal growth and in future therapies.

2024-03-11 | GSE235779 | GEO

Lineage Tracing of RGS5-CreER-Labeled Cells in Long Bones During Homeostasis and Injury.

Project description:Regulator of G protein signaling 5 (RGS5) is a GTPase activator for heterotrimeric G-protein α-subunits, shown to be a marker of pericytes. Bone marrow stromal cell population (BMSCs) is heterogeneous. Populations of mesenchymal progenitors, cells supportive of hematopoiesis, and stromal cells regulating bone remodeling have been recently identified. Periosteal and bone marrow mesenchymal stem cells (MSCs) are participating in fracture healing, but it is difficult to distinguish the source of cells within the callus. Considering that perivascular cells exert osteoprogenitor potential, we generated an RGS5 transgenic mouse model (Rgs5-CreER) which when crossed with Ai9 reporter animals (Rgs5/Tomato), is suitable for lineage tracing during growth and post-injury. Flow cytometry analysis and histology confirmed the presence of Rgs5/Tomato+ cells within CD31+ endothelial, CD45+ hematopoietic, and CD31-CD45- mesenchymal/perivascular cells. A tamoxifen chase showed expansion of Rgs5/Tomato+ cells expressing osterix within the trabeculae positioned between mineralized matrix and vasculature. Long-term chase showed proportion of Rgs5/Tomato+ cells contributes to mature osteoblasts expressing osteocalcin. Following femoral fracture, Rgs5/Tomato+ cells are observed around newly formed bone within the BM cavity and expressed osterix and osteocalcin, while contribution within periosteum was low and limited to fibroblastic callus with very few positive chondrocytes. In addition, BM injury model confirmed that RGS5-Cre labels population of BMSCs expands during injury and participates in osteogenesis. Under homeostatic conditions, lineage-traced RGS5 cells within the trabecular area demonstrate osteoprogenitor capacity that in an injury model contributes to new bone formation primarily within the BM niche.

| S-EPMC10183968 | biostudies-literature

RNA-seq of Procr-expressing mouse mammary myoepithelium

Project description:Procr, also known as EPCR, is a protein C receptor known to function in the platelet coagulation cascade. We have used RNA-seq to examine RNA differential expression between Procr+ and Procr- myoepithelium in mouse mammary gland. Examine RNA differential expression among subsets of freshly sorted mouse mammary gland myoepithelium.

2014-10-31 | E-GEOD-58088 | biostudies-arrayexpress

The IFITM5 mutation in osteogenesis imperfecta type V is associated with an ERK/SOX9-dependent osteoprogenitor differentiation defect

Project description:Osteogenesis imperfecta (OI) type V is the second most common form of OI, distinguished by hyperplastic callus formation and calcification of the interosseous membranes in addition to bone fragility. All patients carry a dominant pathogenic variant (c.-14C>T) in IFITM5. Here, we generated a conditional Rosa26 knock-in mouse model to study the mechanistic consequences of the recurrent mutation. Expression of the mutant Ifitm5 in osteo-chondroprogenitor or chondrogenic cells resulted in low bone mass and growth retardation. Mutant limbs showed impaired endochondral ossification, cartilage overgrowth, and abnormal growth plate architecture. The cartilage phenotype correlates with the pathology reported in OI type V patients. Surprisingly, expression of mutant Ifitm5 in matrix-synthesizing or mature osteoblasts caused no obvious skeletal abnormalities. In contrast, earlier expression in osteo-chondroprogenitors was associated with increase in the skeletal progenitor population within the periosteum. Mutant IFITM5 disrupts early skeletal homeostasis in part by activating ERK signaling and downstream SOX9 protein, and inhibition of these pathways partially rescued the phenotype in mutant animals. . Tracing of chondrogenic cells expressing the mutant Ifitm5 using the Ai9 reporter showed retention of Ai9+ cells in the growth plate and delayed migration to the bone shaft. RNA sequencing demonstrated enrichment for chondrogenic markers in the bone. These data identify the contribution of a defect in osteo-chondroprogenitor differentiation and not osteoblast function as a driver in the pathogenesis of OI type V.

2024-07-23 | GSE268601 | GEO

Il-1β Promotes Superficial Zone Cells Senescence in Articular Cartilage by Inhibiting Autophagy.

Project description:ObjectiveThe superficial zone cells in articular cartilage (SFZCs) have been identified as stem/progenitor chondrocytes and promoted cell self-renewal in the osteoarthritis (OA). Several studies emphasized the involvement of senescence and autophagy in OA. Interleukin-1β (IL-1β) is one of the main inflammatory mediators of OA, and whether it induces senescence and autophagy in SFZCs remains unclear. The present study aimed to investigate autophagy flux, mitochondrial function, and intracellular reactive oxygen species (ROS) that resulted in senescence in SFZCs induced by IL-1β.MethodsUsing western blotting, reverse transcription-quantitative PCR, immunofluorescence, intracellular ROS detection, mitochondrial staining, and determination of mitochondrial membrane potential, we tested senescence and autophagy markers in SFZCs induced by IL-1β in vitro. The consequences of mitochondrial function and ROS were also studied with IL-1β-induced senescence.ResultsIL-1β treatment decreased SFZC proliferation, induced SFZC senescence, and reduced SFZCs' chondrogenic differentiation capacity. Moreover, IL-1β impaired autophagy flux, and the autophagy activator, rapamycin, attenuated the senescence of SFZCs. IL-1β-induced autophagy defect resulted in mitochondrial dysfunction and overproduction of ROS, and autophagy activation notably protected against mitochondrial dysfunction and reduced the levels of ROS. Moreover, antioxidant N-acetylcysteine reversed the senescence of IL-1β in SFZCs.ConclusionIL-1β promotes autophagy impairment and subsequently results in dysfunctional mitochondria and overproduction of ROS, which finally causes SFZC senescence.

| S-EPMC11523166 | biostudies-literature

RNA-seq of Procr-expressing mouse mammary myoepithelium

2014-10-31 | GSE58088 | GEO

PROCR diminishes the efficacy of radiation by impairing T cell-mediated antitumour immunity

Project description:We found that PROCR promotes IL-6 secretion, which is magnified after radiation, leading to inhibition of antitumour immunity. Next, we investigated the mechanism by which PROCR upregulated IL-6. To this end, we performed RNA sequencing on irradiated HONE1 cells with or without PROCR knockout.

2025-05-29 | GSE282897 | GEO

RNA-seq of Procr expressing mouse vascular endothelial cells

Project description:We have used RNA-seq to examine RNA differential expression between Procr+ and Procr- vascular endothelial cells in mouse mammary gland

2016-10-31 | GSE69129 | GEO

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