ScRNA-seq reveals transcriptional profiling of telocytes in synovial tissue
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE303999 | GEO | 2026/02/13
REPOSITORIES: GEO
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Project description:scRNA-seq reveals transcriptional profiling of telocytes in synovial tissue
| PRJNA1298607 | ENA
Project description:Primary telocytes from ankle joints of Efhd1CreER x Ai9 mice were purified by FACS based on tdTomato (tdT) expression. These tdT⁺ telocytes were cultured on collagen-coated CytoSoft® plates of varying stiffness (0.2, 8, and 64 kPa). After 24 hours, cells were harvested for bulk RNA sequencing using Illumina NovaSeq X Plus. The expression of telocyte markers and fibroblast/myofibroblast markers showed stiffness-dependent changes. Notably, stiff ECM induced a telocyte-to-myofibroblast transition, evidenced by downregulation of Efhd1 and Myoc and upregulation of myofibroblast markers(eg. Acta2 and Tagln). Additional analysis revealed significant changes in expression of Timp, Mmp, and Collagen genes. These findings suggest that ECM stiffness is a key regulator of telocyte fate and function at the PLV surface.
2026-02-13 | GSE303624 | GEO
Project description:Marked changes in synovial tissue are seen in knee osteoarthritis and are related to pain; however, the regulation of these processes are not fully understood. Spatial profiling was used to characterize cellular profiles and biological processes within important microenvironments in the synovium (intimal lining, sub-lining, and vessels) between patients that experience more pain compared to those that experience less pain.
2025-04-21 | GSE248454 | GEO
Project description:Background: 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 transcriptomes, compared to synovial tissue from sites not associated with pain. A further aim was to compare differences between early and end-stage disease synovial fibroblasts. Methods: Patients with early knee OA (n=29) and end-stage knee OA (n=22) were recruited. Patient reported pain was recorded by questionnaire and using an anatomical knee pain map. Proton density fat suppressed MRI axial and sagittal sequences were analysed and scored for synovitis. Synovial tissue was obtained from the medial and lateral parapatellar and suprapatellar sites. RNA sequencing was performed using Illumina’s NextSeq 500 and analysed with Galaxy web platform, usegalaxy.org, and Qlucore software. Transcriptomes were functionally characterised using Ingenuity Pathway Analysis. Findings: Parapatellar synovitis was significantly associated with increased OA pain perception. Functional pathway analysis revealed that early OA painful sites mediate immune cell recruitment and promote the formation and development of neurites. Conclusion: OA disease progression and the presence of pain in early OA is associated with different synovial pathotypes. Further interrogation of these pathotypes will increase our understanding of the role of synovitis in OA joint pain and provide a rationale for the therapeutic targeting to alleviate pain in patients.
2021-10-20 | GSE176223 | GEO
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.
2021-10-20 | GSE176308 | GEO
Project description:We have compared synovial biopsies from ankylosing spondylitis and undifferentiated spondylitis patients with healthy controls and osteoarthritis patients Objective: In spondylarthropies, whole-genome gene expression profiling studies have been limited to peripheral blood to date. By undertaking a study in knee synovial biopsies from spondylarthropy (SpA) and ankylosing spondylitis (AS) patients we aimed to identified joint-specific candidate genes and pathways. These pathways may mediate systemic inflammation driven joint damaging processes and more specifically, the osteoproliferation that is characteristic of these conditions. Methods: RNA was extracted from six seronegative SpA, two AS, three osteoarthritis (OA) and four normal control knee synovial biopsies. Whole genome expression profiling was undertaken using the Illumina DASL system, which assays 24000 cDNA probes. Differentially expressed candidate genes were then validated using quantitative PCR and immunohistochemistry. Results: 416 differentially expressed genes were identified that clearly delineated between AS/SpA and control groups. Pathway analysis showed altered gene-expression in oxidoreductase activity, osteoblast activity, B-cell associated, matrix catabolic, and metabolic pathways. The inflammatory mediator, MMP3, was strongly upregulated in AS/SpA samples and the Wnt pathway inhibitors DKK3 and Kremen1 were downregulated. Conclusion: Pathways mediating both systemic inflammation as well as local tissue changes were identified. This suggests initial systemic inflammation in spondylarthropies transfers to and persists in the local joint environment, subsequently mediating changes in genes directly involved in the destructive tissue remodelling. Fifteen knee synovial biopsy tissue samples consisting of six seronegative spondyloarthropy (SpA), two ankylosing spondylitis (AS), three osteoarthritis (OA) and four normal control biopsies were obtained from the Synovial Tissue Bank at the Repatriation General Hospital in Adelaide, South Australia with the appropriate ethical approval (Supplementary Table 1). All patients provided informed written consent.
2012-12-01 | E-GEOD-41038 | biostudies-arrayexpress
Project description:The aim of this study was to compare the gene expression pattern of synovial cells from inflammatory (I) or normal/reactive (N/R) areas of a synovial membrane harvested from the same osteoarthritis (OA) patient. This study is the first to identify different expression pattern between two areas of the synovial membrane in the same patient. These differences concern several key pathways involved in OA pathogenesis (inflammation, cartilage metabolism, Wnt signaling and angiogenesis). This analysis also provides interesting information regarding new potent intermediates as potentiel targets for the future therapeutic. Synovial tissues were obtained from 12 knee OA patients at the time of total knee replacement. The inflammatory status of the synovial membrane was characterized according to macroscopic criteria and sorted as N/R and I. Biopsies were cultured separately for 7 days. Microarray gene expression profiling between N/R and I areas was performed.
2013-05-20 | E-GEOD-46750 | biostudies-arrayexpress
Project description:To investigate differences in gene expression of synovial macrophages in experimental rat knee post traumatic osteoarthritis.
2024-03-22 | GSE216932 | GEO
Project description:The intestinal telocytes that reside beneath the intestinal epithelium exert niche-supporting roles for intestinal stem cells (ISCs) and their progenies. They are heterogenous cells compartmentalized along the crypt-villus axis, but the lineage relationships and mechanisms governing the maintenance of this telocyte population remain poorly understood. Through single cell analysis of mouse small intestine development, here we identify a distinct subset of Foxl1+ mesenchymal cells marked by LIM Domain Only 3 (Lmo3), whose emergence at embryonic day E13.5-14.5 precedes the initiation of villus morphogenesis and the appearance of Lgr5+ ISCs. Later on, these villus-associated telocytes undergo proliferation and expansion, extending their presence to both villus and intervillus regions. After birth, the distribution of the Lmo3+ telocytes gradually becomes confined to the isthmus region, where they persist as long-lived cells and slowly give rise to the progenies that migrate either up- or down-wards and differentiate into villus- or crypt-associated telocytes, respectively. The Lmo3+ cells are responsive to intestinal damage and ablation of these cells compromises the epithelial repair process. Thus, the Lmo3+ cells residing in the isthmus region of the adult small intestine represent a population of telocyte stem cells (TeloSCs) that regulate telocyte niche homeostasis and regeneration. The single cell delineation of the ISC niche emergence and the discovery of TeloSCs open up new avenues for understanding the roles of the mesenchymal environment in intestinal development and diseases.
2025-08-19 | GSE252975 | GEO
Project description:Telocytes regulate tissue resident macrophages in periodontal disease
| PRJNA705494 | ENA