Supersulfides contribute to joint homeostasis and bone regeneration
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1176565 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31094295_1.fastq.gz | Fastqsanger.gz | |||
| SRR31094295_2.fastq.gz | Fastqsanger.gz | |||
| SRR31094296_1.fastq.gz | Fastqsanger.gz | |||
| SRR31094296_2.fastq.gz | Fastqsanger.gz | |||
| SRR31094297_1.fastq.gz | Fastqsanger.gz |
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Project description:The physiological functions of supersulfides, inorganic and organic sulfides with sulfur catenation, have been thoroughly studied. Cysteinyl-tRNA synthetase (CARS2) is the principal supersulfide-producing enzyme. We investigated the role of supersulfides in joint homeostasis and bone regeneration.
2025-03-19 | GSE280156 | GEO
Project description:The physiological functions of supersulfides, inorganic and organic sulfides with sulfur catenation, have been extensively studied. Their synthesis is mainly mediated by mitochondrial cysteinyl-tRNA synthetase (CARS2) that functions as a principal cysteine persulfide synthase. This study aimed to investigate the role of supersulfides in joint homeostasis and bone regeneration. Using Cars2AINK/+ mutant mice, in which the KIIK motif of CARS2 essential for supersulfide production was replaced with AINK, we evaluated the role of supersulfides in fracture healing and cartilage homeostasis during osteoarthritis (OA). Tibial fracture surgery was performed on the wild-type (Cars2+/+) and Cars2AINK/+ mice littermates. Bulk RNA-seq analysis for the osteochondral regeneration in the fracture model showed increased inflammatory markers and reduced osteogenic factors, indicative of impaired bone regeneration, in Cars2AINK/+ mice. Destabilization of the medial meniscus (DMM) surgery was performed to produce the mouse OA model. Histological analyses with Osteoarthritis Research Society International and synovitis scores revealed accelerated OA progression in Cars2AINK/+ mice compared with that in Cars2+/+ mice. To assess the effects of supersulfides on OA progression, glutathione trisulfide (GSSSG) or saline was periodically injected into the mouse knee joints after the DMM surgery. Thus, supersulfides derived from CARS2 and GSSSG exogenously administered significantly inhibited inflammation and lipid peroxidation of the joint cartilage, possibly through suppression of ferroptosis, during OA development. This study represents a significant advancement in understanding anti-inflammatory and anti-oxidant functions of supersulfides in skeletal tissues and may have a clinical relevance for the bone healing and OA therapeutics.
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Project description:Bone fracture healing requires skeletal stem cells (SSCs), which facilitate intramembranous ossification and endochondral ossification in long bone fractures. Although the periosteum is necessary for bone homeostasis and regeneration, the in vivo origin and regulatory mechanisms of periosteal SSCs (P-SSCs) remain unclear. Here, we identified Postn+ P-SSCs at the cambium layer of the periosteum that actively orchestrate regeneration in response to bone injury. Notably, the Postn+ P-SSCs that arise during bicortical fractures are likely derived from Gli1+ P-SSCs. In addition, Postn+ cell ablation compromises cortical bone homeostasis and bone regeneration. The IGF signal is indispensable in the regulatory effect of Postn+ P-SSCs on bicortical fractures since the genetic deletion of Igf1r in Postn+ cells dampens bone fracture healing. Taken together, adult Postn+ cells are region-specific P-SSCs that contribute to bone homeostasis and regeneration and are partially dependent upon IGF signaling.
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Project description:Tcf21+ mesenchymal cells contribute to testis somatic cell development, homeostasis, and regeneration
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Project description:The project investigated chirality-biased proteome during the early stage of bone regeneration on day 3 and day 7.
2023-07-12 | PXD043696 |
Project description:Purpose: Investigate the transcriptomic landscape throughout the time course of murine digit regeneration after level-dependent amputation. Methods: The terminal phalanx bone of hind limb digits was subjected to either a distal amputation (25% bone length loss) or proximal amputation (65% bone length loss). Total RNA was isolated from bone and fibrous tissues distal to the distal interphalangeal joint at 12, 14, and 21 days post-amputation (DPA). mRNA library was sequenced using Illumina HiSeq 3000. Trimmed reads were aligned to the mouse genome mm10 and batch-corrected. Results: A limb-specific developmental signaling pathway is transiently upregulated at 14 DPA after distal amputation, corresponding with regeneration of digit tip tissues. Absence of a limb-specific pathway after proximal amputation corresponded with minimal regeneration and fibrotic scarring. Conclusions: Digit regeneration is a level-dependent and spatiotemporally controlled process, with distal and proximal amputations showing significant differences in gene expression and tissue regrowth over time.
2020-06-10 | GSE131078 | GEO
Project description:Peripheral innervation plays an important role in regulating tissue repair and regeneration. Here, we provide evidence that injured peripheral nerves provide a reservoir of mesenchymal precursor cells that can directly contribute to murine digit tip regeneration and skin repair. In particular, using single-cell RNA sequencing and lineage tracing we identify transcriptionally-distinct mesenchymal cell populations within the control and injured adult nerve, including neural crest-derived cells in the endoneurium with characteristics of mesenchymal precursor cells. Culture and transplantation studies show that these nerve-derived mesenchymal cells have the potential to differentiate into non-nerve lineages. Moreover, following digit tip amputation, the neural crest-derived nerve mesenchymal cells contribute to the regenerative blastema and ultimately to the regenerated bone. Similarly, neural crest derived nerve mesenchymal cells contribute to the dermis during skin wound healing. These findings support a model where peripheral nerves directly contribute mesenchymal precursor cells to promote repair and regeneration of injured mammalian tissues.
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Project description:Lipids play a crucial role in signalling and metabolism, regulating the development and maintenance of the skeleton. Membrane lipids have been hypothesised to act as intermediates upstream of orphan phosphatase 1 (PHOSPHO1), a major contributor to phosphate generation required for bone mineralisation. Here, we spatially resolve the lipid atlas of the healthy mouse knee and demonstrate the effects of PHOSPHO1 ablation on the growth plate lipidome. Lipids spanning 17 subclasses were mapped across the knee joints of healthy juvenile and adult mice using matrix-assisted laser desorption ionisation imaging mass spectrometry (MALDI-IMS), with annotation supported by shotgun lipidomics. Multivariate analysis identified 96 and 80 lipid ions with differential abundances across joint tissues in juvenile and adult mice respectively. In both ages, marrow was enriched in phospholipid platelet activating factors (PAFs) and related metabolites, cortical bone had a low lipid content, while lysophospholipids were strikingly enriched in the growth plate, an active site of mineralisation and PHOSPHO1 activity. Spatially-resolved profiling of PHOSPHO1-knockout (KO) mice across the resting, proliferating, and hypertrophic growth plate zones revealed 272, 306, and 296 significantly upregulated, and 155, 220 and 190 significantly downregulated features, respectively, relative to wild type (WT) controls. Of note, phosphatidylcholine, lysophosphatidylcholine, sphingomyelin, lysophosphatidylethanolamine and phosphatidylethanolamine derived lipid ions were upregulated in PHOSPHO1-KO versus WT. Our imaging pipeline has established a spatially-resolved lipid signature of joint tissues and has demonstrated that PHOSPHO1 ablation significantly alters the growth plate lipidome, highlighting an essential role of the PHOSPHO1-mediated membrane phospholipid metabolism in lipid and bone homeostasis.
2023-04-19 | PXD038909 | Pride
Project description:Peterson2010 - integrated calcium homeostasis
and bone remodelling
This model is described in the article:
A physiologically based
mathematical model of integrated calcium homeostasis and bone
remodeling.
Peterson MC, Riggs MM.
Bone 2010 Jan; 46(1): 49-63
Abstract:
Bone biology is physiologically complex and intimately
linked to calcium homeostasis. The literature provides a wealth
of qualitative and/or quantitative descriptions of cellular
mechanisms, bone dynamics, associated organ dynamics, related
disease sequela, and results of therapeutic interventions. We
present a physiologically based mathematical model of
integrated calcium homeostasis and bone biology constructed
from literature data. The model includes relevant cellular
aspects with major controlling mechanisms for bone remodeling
and calcium homeostasis and appropriately describes a broad
range of clinical and therapeutic conditions. These include
changes in plasma parathyroid hormone (PTH), calcitriol,
calcium and phosphate (PO4), and bone-remodeling markers as
manifested by hypoparathyroidism and hyperparathyroidism, renal
insufficiency, daily PTH 1-34 administration, and receptor
activator of NF-kappaB ligand (RANKL) inhibition. This model
highlights the utility of systems approaches to physiologic
modeling in the bone field. The presented bone and calcium
homeostasis model provides an integrated mathematical construct
to conduct hypothesis testing of influential system aspects, to
visualize elements of this complex endocrine system, and to
continue to build upon iteratively with the results of ongoing
scientific research.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000613.
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2024-09-02 | BIOMD0000000613 | BioModels