Gene expression profiling of adult chondrocyte populations
Ontology highlight
ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE111849 | GEO | 2019/04/23
REPOSITORIES: GEO
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Project description:We profiled gene expression of purified cell types isolated from 5 musculoskeletal tissues: tendon, bone, muscle, cartilage and ligament. We then performed WGCNA to identify tissue-specific transcription factors, signaling pathways and cell surface receptors. The sequencing data for muscle cells is made available here.
2018-03-29 | GSE106292 | GEO
Project description:Ectopic endochondral ossification in the tendon/ligament is caused by repetitive mechanical overload or inflammation. Tendon stem/progenitor cells (TSPCs) contribute to tissue repair and lubrication by producing proteoglycan 4 (Prg4). However, the mechanisms of ectopic ossification and association of TSPCs are not yet known. Here, we investigated the characteristics of Prg4-positive (+) cells and identified that R-spondin 2 (RSPO2), a WNT activator, is specifically expressed in a distinct Prg4+ TSPC cluster. The Rspo2+ cluster was characterized as mostly undifferentiated, and RSPO2 overexpression suppressed ectopic ossification in a mouse Achilles tendon puncture model via chondrogenic differentiation suppression. RSPO2 expression levels in patients with ossification of the posterior longitudinal ligament were lower than those in spondylosis patients, and RSPO2 protein suppressed chondrogenic differentiation of human ligament cells. RSPO2 was induced by inflammatory stimulation and mechanical loading via nuclear factor-kappa B (NF-κB). Rspo2+ cells may contribute to tendon/ligament homeostasis by suppressing chondrogenic differentiation.
2022-06-24 | GSE188759 | GEO
Project description:Tendons and ligaments are important biological structures in both humans and animals. They are part of dense connective tissue and are crucial to the functioning of the musculoskeletal system. However, they are commonly damaged due to age-related wear and tear, trauma or sports related incidents, which can lead to severe immobility for the individual and can lead to injury of other tissues and development of degenerative joint disease such as osteoarthritis. Tissue engineering can offer great potential in the treatment of tendon and ligament injury by seeking a biological replacement with fully regenerated autologenous tissue. This approach commonly involves an artificial ECM (scaffold) on which cell can proliferate and differentiate with subsequent new tissue generation. Fibrin is a natural scaffold with no expected toxic degradation or inflammatory reaction and can be used as an autologous scaffold for fibroblast from connective tissue to create a three dimensional structure. The purpose of this study was to compare the proteomic differences between native tendon, ligament and 3D tissue engineered tendon and ligament fibrin constructs.
2016-06-27 | PXD003094 | Pride
Project description:An Infinium microarray platform (GPL28271, HorvathMammalMethylChip40) was used to generate DNA methylation data from many tissues from horses We generated DNA methylation data from n=333 horse tissue samples representing tissues. Blood samples were collected via venipuncture into EDTA tubes from across 24 different horse breeds (buffy coat). The other tissues were collected at necropsy. The tissue atlas was generated from two Thoroughbred mares as part of the FAANG initiative 37, with the following tissues profiled: adipose (gluteal), adrenal cortex, blood (PBMCs; only n=1 mare), cartilage (only n=1 mare), cecum, cerebellum (2 samples each from lateral hemisphere and vermis), frontal cortex, duodenum, fibroblast, heart (2 samples each from the right atrium, left atrium, right ventricle, left ventricle), hypothalamus, ileum, jejunum, keratinocyte, kidney (kidney cortex and medulla), lamina, larynx (i.e. cricoarytenoideus dorsalis muscle), liver, lung, mammary gland, mitral valve of the heart, skeletal muscle (gluteal muscle and longissimus muscle), occipital cortex, ovary, parietal cortex, pituitary, sacrocaudalis dorsalis muscle, skin, spinal cord (C1 and T8), spleen, suspensory ligament, temporal cortex, tendon (deep digital flexor tendon and superficial digital flexor tendon), uterus.
2021-11-25 | GSE174767 | GEO
Project description:Despite their important roles in the musculoskeletal system, tendon and ligaments are much less studied comparing to bone, cartilage and muscle. The lack of knowledge in tendon biology severely hinders the understanding of the etiologies of tendon related diseases and development of efficient clinical treatments. In mouse, Scx gene, encoding a Twist family bHLH transcription factor, is expressed in progenitors of all tendons and ligaments, as well as in mature tenocytes. Previous studies show that inactivation of Scx gene results in absence or severe hypoplastia of force transmitting tendons, with muscle anchoring tendons and ligaments are less affected. Here we report a set of ChIPseq data from E13.5 forelimbs of novel Scx-2xFlag tagged mice in which a Scx-Flag fusion protein is expressed recapitulating endogenous Scx expression, and a set of RNAseq data of Scx-GFP positive cells from E13.5 Scx wildtype, E15.5 Scx wildtype and homozygous mutant forelimbs. Using RNAseq and ChIPseq assays, we identify several genes exhibiting Scx-dependent tendon expression druing differentiation, with Scx binding peaks located within their promoter/enhancer regions. Thus these genes may play critical roles in mediating Scx regulated tendon cell differentiation. Our results provide new insights in the mechanisms of tendon development.
2021-06-28 | GSE173428 | GEO
Project description:De- and re-differentiation represent phenotypic transitions that may contribute to loss of function in ageing musculoskeletal tissues. Applying a systems biology network analysis approach to global gene expression profiles derived from common in vitro culture systems (monolayer and three-dimensional cultures) this study demonstrates common regulatory mechanisms governing de- and re-differentiation transitions in cartilage and tendon cells. Furthermore, evidence of convergence of gene expression profiles during monolayer expansion, and the expression of key developmental markers, challenges the physiological relevance of this culture system.
2016-06-01 | E-MTAB-4800 | biostudies-arrayexpress
Project description:Background: Musculoskeletal disorders contribute to a substantial proportion of disability among people worldwide. Anterior cruciate ligament (ACL) tears are among the most frequent knee injuries, and a majority of patients will go on to develop knee osteoarthritis within 10 years. Traditional rehabilitation following injury has limited success restoring muscle strength and mitigating the onset of posttraumatic knee osteoarthritis. Growth differentiation factor 8 (GDF8), or myostatin, is a myokine that has been implicated in the pathogenesis of musculoskeletal degeneration following ACL injury. This study investigated GDF8 levels in injured human skeletal muscle and serum and compared the efficacy of a humanized monoclonal GDF8 antibody against a placebo in a mouse model of injury-induced osteoarthritis (surgically induced ACL tear). Muscle GDF8 peaks rapidly following ACL injury, and early induction of GDF8 in skeletal muscle was predictive of atrophy, weakness and periarticular bone loss in patients six months following surgical ACL reconstruction. GDF8 antibody administration at the time of injury substantially reduced muscle atrophy, weakness and fibrosis in the mouse ACL injury model. GDF8 antibody treatment rescued the skeletal muscle and articular cartilage transcriptomic response to ACL injury and attenuated the severity of injury-induced knee osteoarthritis. Subcutaneous treatment with GDF8 antibody also diminished loss of periarticular bone microarchitecture. Genetic deletion of GDF8 neutralized musculoskeletal deficits in response to ACL injury. Our findings support an opportunity for rapid targeting of GDF8 to enhance functional musculoskeletal injury recovery and mitigate the development posttraumatic knee osteoarthritis, which could substantially reduce the disability burden associated with this injury.
2023-12-06 | GSE230736 | GEO
Project description:Background: Musculoskeletal disorders contribute to a substantial proportion of disability among people worldwide. Anterior cruciate ligament (ACL) tears are among the most frequent knee injuries, and a majority of patients will go on to develop knee osteoarthritis within 10 years. Traditional rehabilitation following injury has limited success restoring muscle strength and mitigating the onset of posttraumatic knee osteoarthritis. Growth differentiation factor 8 (GDF8), or myostatin, is a myokine that has been implicated in the pathogenesis of musculoskeletal degeneration following ACL injury. This study investigated GDF8 levels in injured human skeletal muscle and serum and compared the efficacy of a humanized monoclonal GDF8 antibody against a placebo in a mouse model of injury-induced osteoarthritis (surgically induced ACL tear). Muscle GDF8 peaks rapidly following ACL injury, and early induction of GDF8 in skeletal muscle was predictive of atrophy, weakness and periarticular bone loss in patients six months following surgical ACL reconstruction. GDF8 antibody administration at the time of injury substantially reduced muscle atrophy, weakness and fibrosis in the mouse ACL injury model. GDF8 antibody treatment rescued the skeletal muscle and articular cartilage transcriptomic response to ACL injury and attenuated the severity of injury-induced knee osteoarthritis. Subcutaneous treatment with GDF8 antibody also diminished loss of periarticular bone microarchitecture. Genetic deletion of GDF8 neutralized musculoskeletal deficits in response to ACL injury. Our findings support an opportunity for rapid targeting of GDF8 to enhance functional musculoskeletal injury recovery and mitigate the development posttraumatic knee osteoarthritis, which could substantially reduce the disability burden associated with this injury.
2023-12-06 | GSE230708 | GEO
Project description:Vertebrate muscles and tendons are derived from distinct embryonic origins yet they must interact in order to facilitate muscle contraction and body movements. How robust muscle tendon junctions (MTJs) form to be able to withstand contraction forces is still not understood. Using techniques at a single cell resolution we reexamined the classical view of distinct identities for the tissues composing the musculoskeletal system. We identified fibroblasts that have switched on a myogenic program and demonstrate these dual identity cells fuse into the developing muscle fibers along the MTJs facilitating the introduction of fibroblast-specific transcripts into the elongating myofibers. We suggest this mechanism resulting in a hybrid muscle fiber, primarily along the fiber tips, enables a smooth transition from muscle fiber characteristics towards tendon features essential for forming robust MTJs. We propose that dual characteristics of junctional cells could be a common mechanism for generating stable interactions between tissues throughout the musculoskeletal system.
2021-03-04 | GSE168153 | GEO
Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml) Cartilage was obtained from adult human tissue donors with above the knee amputations due to chondrosarcoma or traumatic injury or from autopsy. Chondrocytes were isolated following established protocols, maintained in high density, and treated with IL-1B (10 ng/ml). Chondrocytes treated with buffer only served as the untreated control. The experiment was carried out in duplicate. Total RNA was extracted from these chondrocytes, labeled with fluorophores (Cy3 or Cy5) and analyzed for expression changes using the Human Operon/Qiagen v3.0 oligonucleotide array. The analysis was repeated with the fluorophore dyes exchanged between the untreated and experimental RNAs.
2008-05-14 | E-GEOD-11427 | biostudies-arrayexpress