Simulated microgravity recapitulates early molecular events and sex differences of knee osteoarthritis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE231848 | GEO | 2024/05/30
REPOSITORIES: GEO
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Project description:Aims：To establish a novel model of mechanical loading-induced knee osteoarthritis (KOA) and explore its regulatory mechanisms through transcriptomics. Methods：Knee joints of Sprague-Dawley (SD) rats were mechanically loaded with 13 N, 20 N and 27 N for 2 or 4 weeks to construct mechanically-induced KOA model. Immunohistochemistry (IHC), quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, Safranin O/fast green staining, enzyme-linked immunosorbent assay (ELISA), micro-computed tomography (Micro-CT) and behavioral analysis were used to evaluate damage on the right knee joint. Transcriptomic analysis combined with validation experiments were performed to explore the regulatory mechanism of excessive mechanical loading on KOA development. Results：A vertical load of 27 N resulted in calf fractures, whereas a 13 N load did not cause remarkable pathological alteration in the knee joint. Notably, applying compression at a load of 20 N for 4 weeks (w) significantly promoted the levels of pro-inflammatory factors IL-6, IL-β and TNF-α in serum and joint fluids and markedly minimized the levels of anti-inflammatory factors IL-10 and TGF-β. Immunohistochemistry, qRT-PCR and Western blot analyses suggested that the 20 N load reduced the expression of anabolism markers (ACAN and COL2A1) and escalated the expression of catabolism markers (MMP13 and ADAMTS4). KEGG analysis and validation results showed that the PIEZ1 channel, Ca2+ signaling pathway, PI3K-AKT signaling pathway and NF-κB signaling pathway were significantly activated in the 20N-4 w group. Conclusion：Continuous loading with 20 N for 4 weeks can induce significant OA-like damage to the cartilage of the right knee in rats, which might be induced through the piezo1-Ca2+/PI3K-AKT/ NF-κB signaling pathway.
2024-09-05 | GSE276365 | GEO
Project description:Background: Meniscus tears are the most common injury in the knee and are associated with an increased risk of osteoarthritis (OA). The molecular profile of knees with meniscus tears is not well-studied. Therefore, to advance our understanding of the early response of the knee to injury, we compared the gene expression profile of meniscus and articular cartilage within the same knees following meniscus injury. Hypothesis/Purpose: To identify differences between the molecular signatures of meniscus and articular cartilage from knees with intact articular cartilage undergoing arthroscopic partial meniscectomy. Study Design: Descriptive laboratory study Methods: Patients (n=12) with a known isolated medial meniscus tear without any knee chondrosis or radiographic OA were consented prior to surgery. During arthroscopic partial meniscectomy, a sample of their injured meniscus and a sample of their articular cartilage off the medial femoral condyle were procured. The transcriptome signatures, as measured through Affymetrix microarray, were compared between the two tissues and underlying biological processes were explored computationally. Results: 3566 gene transcripts were differentially expressed between meniscus and articular cartilage. Gene transcripts down-regulated in articular cartilage were associated with extracellular matrix organization, wound healing, cell adhesion, and chemotaxis. Gene transcripts up-regulated in articular cartilage were associated with blood vessels morphogenesis and angiogenesis. Examples of individual genes with significant differences in expression between the two tissues include IBSP (23.76 fold; P < 0.001), upregulated in meniscus, and TREM1 (3.23 fold; P = 0.006), upregulated in meniscus. Conclusion: The meniscus and articular cartilage have distinct gene expression profiles in knees with meniscus tears and intact articular cartilage. Total RNA obtained from injured meniscus and normal articular cartilage from patients undergoing partial meniscectomy.
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Project description:Synovial inflammation is associated with pain severity in patients with knee osteoarthritis (OA). The aim here was to determine in a population with knee OA, whether synovial tissue from areas associated with pain exhibited different synovial fibroblast subsets, compared to synovial tissue from sites not associated with pain. A further aim was to compare differences between early and end-stage disease synovial fibroblast subsets. Parapatellar synovitis was significantly associated with the pattern of patient-reported pain in knee OA patients. Synovial tissue from sites of patient-reported pain exhibited a differential transcriptomic phenotype, with distinct synovial fibroblast subsets in early OA and end-stage OA. Functional pathway analysis revealed that synovial tissue and fibroblast subsets from painful sites promoted fibrosis, inflammation and the growth and activity of neurons. The secretome of fibroblasts from early OA painful sites induced neurite outgrowth in dorsal root ganglion neurons. Sites of patient-reported pain in knee OA is associated with a different synovial tissue phenotype and distinct synovial fibroblast subsets. Further interrogation of these fibroblast pathotypes will increase our understanding of the role of synovitis in OA joint pain and provide a rationale for the therapeutic targeting of fibroblast subsets to alleviate pain in patients.
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Project description:Osteoarthritis (OA) affects all tissues in the knee joint but therapeutic targets have often been selected for their role in cartilage damage and inflammation and largely omitted consideration of mechanisms that are mediating meniscus damage and more importantly there have been insufficient efforts to determine whether pathogenic processes are shared between tissues. Several scRNA-seq analyses have been performed in OA knees but have been largely restricted to the analysis of a single joint tissue of articular cartilage, or meniscus with the exception of one study that analyzed cartilage and synovium. Here, we performed scRNA-seq analyses of healthy and OA-affected human knee cartilage and menisci to interrogate separate and shared mechanisms in cellular homeostasis and OA pathogenesis.
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Project description:There is a need to clarify the role of the meniscus in knee OA which may be aided by the identification of biomarkers that reflect the molecular events involved in the tissue degradation. This is of particular importance in the early stages of the degenerative processes, a crucial phase when it might still be possible to interfere with disease progression before tearing and critical loss of meniscal function occurs. One way to achieve this goal is exploratory proteomics by mass spectrometry (MS), which has the potential to analyse the proteome of complex samples. Thus, our aim was to gain new knowledge about the molecular processes within the human meniscus by comparing the proteomic profiles of both the lateral and medial meniscus from healthy controls, subjects with mild signs of joint degeneration, and patients with end-stage knee OA, using a non-targeted MS approach operating in data-independent acquisition (DIA) mode. For the research purpose six groups were established: medial and lateral menisci from control donors (n=12), medial and lateral menisci from donors with mild signs of joint degeneration (n=13) and medial and lateral menisci from end-stage knee OA patients (n=12).
2024-04-03 | PXD042122 | Pride
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