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Expression profiling of ankle joint of a mouse model of gouty arthritis uncovers potential mechanisms involved in pain and inflammation

ABSTRACT: Expression profiling of ankle joint of a mouse model of gouty arthritis uncovers potential mechanisms involved in pain and inflammation

PROVIDER: PRJNA1015204 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26027001.fastq.gz	Fastqsanger.gz
	SRR26027002.fastq.gz	Fastqsanger.gz
	SRR26027003.fastq.gz	Fastqsanger.gz
	SRR26027004.fastq.gz	Fastqsanger.gz
	SRR26027005.fastq.gz	Fastqsanger.gz

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Expression profiling of ankle joint of a mouse model of gouty arthritis uncovers potential mechanisms involved in pain and inflammation

Project description:Gout arthritis (GA) is a prevalent and painful inflammatory arthritis, and its global burden continues to rise. Intense pain induced by gout attacks is a major complication of gout. Treatment and long-term management for gout patients remain challenging. However, the pathogenesis of GA still remained largely unknown. The purpose of this study is to perform an expression profiling to identify genes related with GA in an animal model. Using a monosodium urate (MSU) crystals-induced GA model, we performed RNA-sequencing for the ankle joint of gout mice in different time points. Our results revealed transcriptional changes in the joint. We provided by far the first study to profile gene expression changes and pathway analysis of ankle joint in different time for investigating GA mechanisms. This work may provide novel insights into understanding the mysterious mechanisms underlying GA.

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Transcriptional analysis of alveolar bone, jaw and ankle joint in inflammatory arthritis

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2023-04-25 | GSE230178 | GEO

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Multimodal smart systems reprMultimodal smart systems reprogram macrophages and remove urate to treat gouty arthritisogram macrophages and remove urate to treat gouty arthritis

Project description:Gouty arthritis (GA) is a chronic and progressive disease that often develops due to high urate levels, leading to joint damage and characterized by an inflammatory immune microenvironment (IIMe). Quantitative proteomics further revealed D-N camouflaged with hybid membranes of M2 exosome and its parent microphage (D-N[EM2]) treated GA disease mechanisms.

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Project description:Temporomandibular joint (TMJ) osteoarthritis (OA) is a highly prevalent disorder affecting patient’s quality of life due to joint pain and dysfunction. A comprehensive understanding of cell type diversity and their dynamics of TMJ along joint degeneration and pain is lacking. Here we established an inflammatory TMJOA mouse model via intra-articular injection of CFA (Complete Freund’s Adjuvant). TMJOA mice exhibited OA and orofacial pain, recapitulating hallmark symptoms in patients. We performed single-cell transcriptomic profiling of TMJ followed by the validation. We revealed cellular diversity, anatomic position, and cell dynamics of TMJ at single cell resolution along the joint degeneration and pain.

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Project description:Gout is a prevalent and painful inflammatory arthritis, and its global burden continues to rise. Intense pain induced by gout attacks is a major complication of gout. Treatment and long-term management for gout patients remain challenging. Despite the discovery of many key immune response and inflammatory genes and pathways in gout, the molecular mechanisms of gout inflammation are still not entirely elucidated. Particularly, systematic studies of gout inflammation and pain are lacking. Using a monosodium urate (MSU) crystals-induced gout model, we performed genome-wide transcriptome analysis for the ankle joint, dorsal root ganglion (DRG), and spinal cord of gout mice. Our results revealed transcriptional changes in both the joint and the nervous system. Furthermore, through integrated analysis with public datasets of mouse inflammatory pain and neuropathic pain models, human GWAS, osteoarthritis (OA), and rheumatoid arthritis (RA), we identified common and unique features associated with acute gout inflammation and severe pain.

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Project description:Temporomandibular joint (TMJ) arthritis is a craniofacial disorder characterized by joint dysfunction and orofacial pain. Despite of its established roles in fluid and immune regulation, lymphatic regulation, and function in TMJ remain unknown. Using genetic report mouse, uDISCO tissue clearing, and 3D volume imaging, we defined lymphatic vessel morphology, structure, anatomic location in adult mouse TMJ. We demonstrate in a mouse model of TMJ osteoarthritis (TMJOA) that arthritis induces inflammatory lymphangiogenesis and leads to impaired synovial lymphatic functions, including decreases in synovial influx and lymph node fluid drainage. To establish the causative link between lymphatic remodeling and TMJOA, we performed lymphatic loss- and gain-of-function studies. Lymphatic deficiency exacerbated cartilage defects, bone loss, synovitis, synovial fibrosis, and pain behaviors in TMJOA mice. Conversely, lymphatic activation via a hydrogel-mediated VEGF-C delivery to TMJ reduced TMJ pain, inflammation, and arthritis-like pathogenesis. Therefore, we defined lymphatic structure in TMJ and found that lymphatic dysfunction drives TMJOA pathogenesis and pain, suggesting its potential as a therapeutic target.

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Project description:Background: Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease marked by the progressive degeneration of cartilage and underlying bone, resulting in pain and functional impairment. Despite current conservative treatments such as physical therapy and NSAIDs, the etiology and pathophysiology of TMJOA are unclear, making effective management difficult. Finding reliable biomarkers for early identification and new therapeutic targets is crucial to improve treatment outcomes.

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Lymphatic vessels drain monosodium urate and activate immunity in gouty arthritis

Project description:Gouty Arthritis (GA) is caused by urate deposition in the joint capsule, cartilage, bone, and surrounding tissues to trigger recurrent attacks of acute joint inflammation. However, the clearance mechanism of urate deposition is still not clear. We aimed to investigate whether lymphatics vessels can drain monosodium and involve in the immune process of GA. Methods: Inguinal lymph nodes (LNs) in 4 normal volunteers and 4 patients with acute flare of GA were examined by ultrasound. Acute and chronic GA flare mouse models were established by intra-footpad administrations of monosodium urate (MSU) for 1 week or 1 month. Mice were treated with VEGFR-3 inhibitor or undergone popliteal lymph node (PLN) excision or PLN macrophage depletion. The severity of foot inflammation, lymphatic draining function, concentration of uric acid (UA), and macrophage population were examined. Macrophages were co-cultured with MSU-treated lymphatic endothelial cells (LECs) and differential gene expression of LECs was assessed by Agilent gene expression microarray. Results: 1) Draining LNs were enlarged in patients with GA flare and GA mouse models. 2) The lymphatic function and structure were abnormal in GA mouse models. 3) Acute GA mice had elevated UA levels in draining LNs, but not in the serum, while chronic GA mice had elevated UA levels in both LNs and serum. 4) Blockade of VEGFR-3 reduced foot inflammation in chronic GA mice. 5) MSU induces pro-inflammatory polarization of macrophages by inducing LEC inflammation. 6) PLN local depletion of macrophages or removal of PLNs alleviated foot inflammation in GA. Conclusions: Lymphatics drain MSU to the draining LNs to clear deposited urate in the distal extremity and induce LECs to stimulate macrophage pro-inflammatory response during GA. We have identified a novel mechanism about MSU clearance and pro-inflammatory macrophage activation, and provided possible therapeutic approach for GA.

2022-04-02 | GSE199950 | GEO

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