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Transcriptome changes of OA rat synovium before and after the injection of human SyMSCs and AdMSCs

ABSTRACT: Transcriptome changes of OA rat synovium before and after the injection of human SyMSCs and AdMSCs

PROVIDER: PRJNA1052032 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27200066_1.fastq.gz	Fastqsanger.gz
	SRR27200066_2.fastq.gz	Fastqsanger.gz
	SRR27200067_1.fastq.gz	Fastqsanger.gz
	SRR27200067_2.fastq.gz	Fastqsanger.gz
	SRR27200068_1.fastq.gz	Fastqsanger.gz

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Transcriptome changes of OA rat synovium before and after the injection of human SyMSCs and AdMSCs

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Human transcripts up-regulated in the human mesenchymal stem cells migrated within the rat synovium; rat transcripts up-regulated in the rat synovium after human mesenchymal stem cells injection

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Human transcripts up-regulated in the human mesenchymal stem cells migrated within the synovium

Project description:After the injection of human synovial mesenchymal stem cells into the rat (Lewis strain) knee joint, synovium was investigated using species specific microarray analyses of human and rat transcripts to investigate the gene expression change after injection. Human synovial mesenchymal stem cells were injected into the rat anterior cruciate ligament transected knee. After harvesting the synovium and extraction of RNA, species specific microarray analyses were performed uisng Affymetrix microarrays to investigate the gene expression change of human and rat transcripts after injection.

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Human transcripts up-regulated in the human mesenchymal stem cells migrated within the rat synovium rat transcripts up-regulated in the rat synovium after human mesenchymal stem cells injection

Project description:Human transcripts up-regulated in the human mesenchymal stem cells migrated within the rat synovium rat transcripts up-regulated in the rat synovium after human mesenchymal stem cells injection

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Dysregulated gene expression in human osteoarthritic (OA) and rheumatoid arthritis (RA) synovium

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Intraarticular injection of liposomal adenosine reduces cartilage damage in established murine and rat models of osteoarthritis

Project description:Osteoarthritis (OA) affects nearly 10% of the population of the United States and other industrialized countries and, at present, short of surgical joint replacement, there is no therapy available that can reverse the progression of the disease OA. Adenosine, acting at its A2A receptor (A2AR), is a critical autocrine factor for maintenance of cartilage homeostasis. Here we report that injection of liposomal suspensions of a selective A2AR agonist, CGS21680, significantly reduced OA cartilage damage in a rat model of established post-traumatic OA (PTOA). Differential expression analysis of mRNA from chondrocytes harvested from knees of rats with PTOA treated with liposomal A2AR agonist revealed downregulation of genes associated with matrix degradation and upregulation of genes associated with cell proliferation as compared to liposomes alone.

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Project description:Objectives : Joint pain causes a significant morbidity in osteoarthritis (OA). The synovium as an innervated joint structure might contribute to the peripheral pain in OA. Methods : We used a hypothesis-free next generation RNA sequencing to study protein coding and small non-coding transcriptomes in knee synovial tissues of OA patients (n=10) with high and low knee pain (evaluated by visual analogue scale) followed by Gene Ontology (GO) and pathway analyses and integration of mRNAs and small RNAs data sets. Results : We showed that 33 protein-coding genes and 35 small RNAs were differentially expressed in the knee synovium of patients with high compared to low intensity knee pain, with 30 mRNAs and 14 small RNAs being upregulated and 2 mRNAs and 21 small RNAs being downregulated. Top enriched genes, such as SDIM1 and CPE encode neuronal proteins that share molecular properties with neurotrophic factor BDNF and promote neuronal survival under cellular stress, and OTOF participates in calcium-dependent synaptic exocytosis and modulation of GABAergic activity. TrkB was enriched in several gene networks, suggesting its key role in pain-related transcriptional changes in OA joint. Downregulation of PTX3 in high pain group supports an argument that inflammation and pain are independent processes in symptomatic knee OA. MiR-146a-3p and miR150 appeared as the microRNA candidates in the pathogenesis of OA-related knee pain. Conclusions : Here we uncovered the molecular complexity of pain-related transcriptome changes in the synovium of knee joints in osteoarthritis. We identified new molecular candidates in OA pain setting a firm ground for future mechanistic studies and drug discovery in OA.

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