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Understanding downstream signaling pathways regulated by miR-34a-5p in articular cartilage by RNA sequencing using miR-34a knock-out mice

ABSTRACT: Understanding downstream signaling pathways regulated by miR-34a-5p in articular cartilage by RNA sequencing using miR-34a knock-out mice

PROVIDER: PRJNA552531 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9640990_1.fastq.gz	Fastqsanger.gz
	SRR9640990_2.fastq.gz	Fastqsanger.gz
	SRR9640991_1.fastq.gz	Fastqsanger.gz
	SRR9640991_2.fastq.gz	Fastqsanger.gz
	SRR9640992_1.fastq.gz	Fastqsanger.gz

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Understanding downstream signaling pathways regulated by miR-34a-5p in articular cartilage by RNA sequencing using miR-34a knock-out mice

Project description:The goal of this study was to determine the role of miR-34a in regulating chondrocyte transcript profiles. Next Generation Sequencing of total RNA extracted from mouse KO and WT chondrocytes revealed 175 significantly differentially expressed genes (84 up, 91 down) in miR-34a KO chondrocytes compared to WT cells. We are currently validating potential direct targets of miR-34a from our NGS data and performing computational pathway analysis to identify novel pathways regulated by miR-34a.

2021-03-08 | GSE133775 | GEO

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Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

2019-10-14 | PXD015278 | Pride

Expression data from articular and growth plate cartilage

Project description:The aim of the current study was to identify molecular markers for articular cartilage that can be used for the quality control of tissue engineered cartilage. Therefore a genom-wide expression analysis was performed using RNA isolated from articular and growth plate cartilage, both extracted from the knee joints of minipigs. Keywords: Native material or primary cells isolated from articular cartilage and growth plate cartilage Articular and growth plate cartilage were taken for RNA extraction and hybridization on Affymetrix microarrays. Furthermore chondrocytes from each type of cartilage were isolated and cell culture was started and terminated at day 10 or day 20. Total RNA from cultivated cells was extracted, and hybridization on Affymetrix microarrays was performed.

2011-07-28 | E-GEOD-23492 | biostudies-arrayexpress

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Project description:Chondrocyte gene expression was analyzed to study mechanisms involved in the structural and functional adaptation of articular cartilage during postnatal maturation. Transcriptional profiling was used to compare articular chondrocytes between four neonatal and four adult horses. Expressional differences featured matrix proteins and matrix-modifying enzymes reflecting the transition from cartilage growth to cartilage homeostasis. Keywords: articular cartilage, maturation, horse, cDNA microarray

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Project description:Articular cartilage is deprived of blood vessels and nerves, and the only cells residing in this tissue are chondrocytes. The molecular properties of the articular cartilage and the architecture of the extracellular matrix demonstrate a complex structure that differentiates on the depth of tissue. Osteoarthritis (OA) is a degenerative joint disease, the most common form of arthritis, affecting the whole joint. It is associated with ageing and affects the joints that have been continually stressed throughout life including the knees, hips, fingers, and lower spine region. OA is a multifactorial condition of joint characterised by articular cartilage loss, subchondral bone sclerosis, and inflammation leading to progressive joint degradation, structural alterations, loss of mobility and pain. Articular cartilage biology is well studied with a focus on musculoskeletal diseases and cartilage development. However, there are relatively few studies focusing on zonal changes in the cartilage during osteoarthritis.

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Project description:To reveal the potential regulation target genes of miR-26a and miR-23a/b clusters in articular chondrocytes, we performed a multi-omics analysis of LC-MSMS and RNA-seq using cultured chondrocytes samples, which were primarily isolated from 3-week-old wild-type, miR-26a -/- (with or without miR-26a mimic transfection afterwards) or miR-23a/b cluster flox/flox;Col2a1-cre mice. For LC-MSMS, protein from TRIZOL reagent was extracted, nanoLC-MSMS was performed. An expression list was made to further explore the regulation targets of miR-26a and miR-23a/b clusters.

2023-01-25 | PXD031868 | Pride

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