Biomarker Discovery in Knee Osteoarthritis (I)
Ontology highlight
ABSTRACT:
ORGANISM(S): Human Homo Sapiens
TISSUE(S): Urine
DISEASE(S): Osteoarthritis
SUBMITTER: 
Susan Sumner
PROVIDER: ST000020 | MetabolomicsWorkbench | Fri Feb 28 00:00:00 GMT 2014
REPOSITORIES: MetabolomicsWorkbench
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| mwtab | Other |
Items per page: 5 1 - 1 of 1 |
Similar Datasets
Project description:This metabolomics pilot and feasibility (P & F) study was conducted to provide data to be used to gain a better understanding of metabolic alterations in people with knee osteoarthritis (OA) and to discover novel biomarkers of the disease. The goal of the metabolomics study was to determine if metabolic differences, detected by a comprehensive metabolomics analysis, can be used to distinguish people who will develop symptomatic knee OA from those who will not. For this metabolomics study, individuals participating in T1 or T1* with 5-year follow-up at T2 were selected. At T2 subjects were on average 68.1(9.12) years old with an average BMI of 31.4(7.01) with 32% men and one-third African American. All had weight-bearing posterior-anterior knee films obtained with the Synaflexer positioning device at both time points and read paired for Kellgren-Lawrence grade and minimum joint space. Urine samples (second morning void) collected from 36 overweight or obese participants in the JoCo at T1 or T1* were selected from two subgroups (a group that developed radiographic osteoarthritis (n=16) and an age, race, sex, and BMI matched group that did not develop osteoarthritis (n=20). Radiographic knee OA was defined as Kellgren-Lawrence grade 2-4 at T2 in a person with Kellgren-Lawrence grade 0 or 1 at T1 or T1*.
2014-03-04 | ST000022 | MetabolomicsWorkbench
Project description:<p>The Osteoarthritis Initiative (OAI) is a publicly and privately funded prospective longitudinal cohort with a primary objective of identifying risk factors for incidence and progression of tibiofemoral knee OA. The OAI utilized a focused population-based recruitment to enroll 4,674 men and women between the ages of 45-79 years who either had radiographic symptomatic knee OA or who were without radiographic symptomatic OA in both knees but were considered high risk for OA because they had two or more known risk factors for knee OA. Subjects were recruited into the baseline phase of the OAI at multiple sites throughout the US between 2004 and 2006. All subjects were invited back for follow-up examinations to assess incidence or progression of OA annually, for up to 5 years.</p> <p>Phenotype data from the baseline and follow-up examinations are available for public access from the Osteoarthritis Initiative (OAI) database at <a href="http://www.oai.ucsf.edu/">http://www.oai.ucsf.edu/</a>. </p> <p>The Genetic Components of Knee Osteoarthritis (GeCKO) Study was initiated in 2009 as a genetic ancillary study to perform a genome-wide association study to identify genetic variants associated with radiographic osteoarthritis. This study included 4,482 individuals participating in the parent OAI study. Following sample cleaning (e.g., removal of duplicates, sex mismatches, poor sample quality, etc.), the final sample set included 4,129 individuals.</p>
| phs000955 | dbGaP
Project description:Identification of novel synovial fluid biomarkers that can differentiate early changes following ACL injury from OA using tandem-mass-spectrometry
2019-03-11 | MSV000083551 | MassIVE
Project description:Osteoarthritis (OA) is the most prevalent chronic joint disease which increases in frequency with age eventually impacting most people over the age of 65. OA is the leading cause of disability and impaired mobility, yet the pathogenesis of OA remains unclear. Treatments have focused mainly on pain relief and reducing joint swelling. Currently there are no effective treatments to slow the progression of the disease and to prevent irreversible loss of cartilage. Here we demonstrate that stable expression of RORb in cultured cells results in alteration of a gene program that is supportive of chondrogenesis and is protective against development of OA. Specifically, we determined that RORb regulates the balance of FGFRs signaling on FGFR1/FGFR3 that ERK1/2-MAPK signaling was suppressed by FGFR1(cartilage destruction) and AKT signaling was enhanced by FGFR3 (cartilage protection). These results suggest a critical role for RORb in chondrogenesis and suggest that identification of mechanisms that control the expression of RORb in chondrocytes could lead to the development of disease modifying therapies for the treatment of OA
2022-10-19 | GSE208277 | GEO
Project description:Osteoarthritis (OA) is the most common joint disease, affecting over 300 million people world-wide. Accumulating evidence attests to the important roles of immune system in OA pathogenesis. Understanding the role of various immune cells in joint degeneration or joint repair after injury is helpful for improving therapeutic strategies for treating OA. Post-traumatic osteoarthritis (PTOA) develops in ~50% of individuals who have experienced an articular trauma like an anterior cruciate ligament (ACL) rupture. Here, using highly sensitive single-cell RNA sequencing technology, we delineated the temporal dynamics of immune cell accumulation in the mouse knee joint after ACL rupture.
2022-07-18 | GSE200843 | GEO
Project description:Osteoarthritis (OA) is a highly prevalent and morbid disease affecting over 30 million Americans. Effective drugs and treatments to halt the progression or reverse OA pathogenesis are not available, creating a need for translational research in the field. The A2AR null mouse is an important animal model for the understanding of disease pathogenesis and the development of novel therapies. We have previously shown that these mice develop OA spontaneously by age 16 weeks and that liposomal adenosine is able to reverse established OA in animal models of post-traumatic OA and overbearing/overweight OA. We here illustrate how the A2ARKO transcriptome shows early compromise of cell viability and compares to that of human OA chondrocytes.
2020-09-01 | GSE146349 | GEO
Project description:Osteoarthritis causes pain and functional disability for over 500 million people worldwide and characterized by progressive loss of cartilage from the articulating surfaces of diarthrodial joints. Although the etiology of the disease is unknown, it is widely accepted that these degenerative changes arise from an imbalance of synthetic and degradative pathways that control cartilage extracellular matrix metabolism. Genome-wide U133A Affymetrix oligonucleotide array set was used to comprehensively investigate the expression pattern in non-osteoarthritis (normal) and cartilage obtained from OA patients undergoing knee replacement surgery. This study was undertaken to better understand the molecular basis of the disease and to provide relevant insight into phenotypical alterations and mechanisms involved in OA pathogenesis.
2021-03-18 | GSE169077 | GEO
Project description:Osteoarthritis (OA) causes pain and functional disability for over 500 million people worldwide and is characterized by progressive loss of cartilage and synovial hyperplasia from the articulating surfaces of diarthrodial joints. Although the etiology of the disease is unknown, it is widely accepted that these degenerative changes arise from an imbalance of synthetic and degradative pathways that control cartilage and synovium extracellular matrix metabolism. Genome-wide U133A Affymetrix oligonucleotide array set was used to comprehensively investigate the expression pattern in non-osteoarthritis (normal) and synovium obtained from OA and rheumatoid arthritis (RA) patients undergoing knee replacement surgery. This study was undertaken to understand the disease's molecular basis better and provide relevant insight into phenotypical alterations and mechanisms involved in OA pathogenesis.
2022-08-01 | GSE206848 | GEO
Project description:Osteoarthritis (OA) treatment is limited by the lack of effective non-surgical interventions to slow disease progression. Here, we examined the contributions of the subchondral bone properties to OA development. We used parathyroid hormone (PTH) to modulate bone mass prior to OA initiation and alendronate (ALN) to inhibit bone remodeling during OA progression. We examined the spatiotemporal progression of joint damage by combining histopathological and transcriptomic analyses across joint tissues. The additive effect of PTH pretreatment prior to OA initiation and ALN treatment during OA progression most effectively attenuated load-induced OA pathology. Individually, PTH directly improved cartilage health and slowed the development of cartilage damage, whereas ALN primarily attenuated subchondral bone changes associated with OA progression. Joint damage reflected early transcriptomic changes. With both treatments the structural changes were associated with early modulation of immunoregulation and -response pathways that may contribute to disease mechanisms. Overall, our results demonstrate the potential of subchondral bone-modifying therapies to slow the progression of OA.
2024-01-31 | GSE253303 | GEO
Project description:Osteoarthritis (OA) is the most common joint disease and is the leading cause of chronic disability among older people. Chondrocyte death was involved in OA pathogenesis. Ferroptosis is an iron-dependent cell death associated with peroxidation of lipids. Expression of GPX4 in the OA cartilage from OA patients were significantly lower than normal cartilage.In order to analyze the mechanism of GPX4, we conducted RNA-sequencing in mouse chondrocytes with or without GPX4 knockdown.Our results showed that Gpx4 downregulation could increase the sensitivity of chondrocytes to oxidative stress and aggravate ECM degradation in chondrocytes.
2022-02-18 | GSE190184 | GEO