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MicroRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (RNA-seq)

ABSTRACT: RNA-seq of RNA isolated form costal chondrocytes of mice at post-natal day 7

ORGANISM(S): Mus musculus

PROVIDER: GSE144360 | GEO | 2020/07/17

REPOSITORIES: GEO

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microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (Illumina HT12v4 expression arrays)

Project description:MiR-140 is selectively expressed in cartilage. Deletion of the entire miR-140 locus in mice results in a growth retardation phenotype and an early-onset osteoarthritis-like pathology, however the relative contribution of miR-140-5p or miR-140-3p to the phenotype remains to be determined. An unbiased small RNA sequencing approach identified that miR-140-3p was in vast abundance (>10-fold) to miR-140-5p in human cartilage. Analysis of these data identified multiple miR-140-3p isomiRs differing from the miRBase [1] annotation at both the 5´ and 3´ end, with >99% of miR-140-3p isomiRs having one of two ‘seed’ sequences (5´ bases 2-8). The most abundant isomiR with each seed were selected for further analysis; miR-140-3p.2 which has an identical seed to the miRBase miR-140-3p (ACCACAG) and miR-140-3p.1 which has an altered seed (CCACAGG), and thus different potential targets. Each isomiR was overexpressed in chondrocytes and whole-genome transcriptomics used to identify targets. miR-140-3p.1 and miR-140-3p.2 significantly down-regulated 694 and 238 genes respectively (adj.P.Val<0.05), of which only 162 genes were commonly down-regulated by both isomiRs. Targets of both isomiRs were validated using 3´UTR luciferase assays. A significant enrichment of miR-140-3p.1 targets was identified within genes whose expression increase in the rib chondrocytes of Mir140-null mice and within genes whose expression decreased during human chondrogenesis. Finally, through imputing the expression of miR-140 from the expression of the host gene WWP2 in 124 previously published datasets an inverse correlation with miR-140-3p.1 predicted targets was identified. Together these data suggest the novel seed containing isomiR miR-140-3p.1 is more functional than the original consensus miR-140-3p or the isomiR with the same seed, miR-140-3p.2.

2020-07-17 | GSE144367 | GEO

microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-07-17 | GSE144374 | GEO

microRNA-seq of cartilage reveals an overabundance of miR-140-3p which contains functional isomiRs.

Project description: Not available

| S-EPMC7566571 | biostudies-literature

microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs

Project description:microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs

| PRJNA603515 | ENA

microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (RNA-seq)

Project description:microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (RNA-seq)

| PRJNA603491 | ENA

microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (Illumina HT12v4 expression arrays)

Project description:microRNA-seq of cartilage reveals an over-abundance of miR-140-3p which contains functional isomiRs (Illumina HT12v4 expression arrays)

| PRJNA603496 | ENA

Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.

2019-08-12 | PXD014988 | Pride

miR-140 deficiency effect on the chondrocytes

2010-01-01 | GSE16007 | GEO

miR-140 deficiency effect on the chondrocytes

Project description:Analysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes. Keywords: Expression profiling by array DNA microarray analysis was performed using Affymetrix mouse genome 430 2.0 array. RNA samples collected from cultured rib chondrocytes of wild-type and miR-140-/- to identify potential mRNA targets of miR-140. 2 M-BM-5g of total RNA was reverse transcribed with SuperScript II and second strand cDNA was synthesized. Biotinylated antisense cRNAs was amplified and transcribed using the GeneChip expression 3M-bM-^@M-^Y-Amplification reagent (Affymetrix). Finally, 10 M-BM-5g of cRNAs were fragmented and hybridized to GeneChip (R) Mouse Genome 430 2.0 array (Affymetrix). Microarray data were summarized by Robust Multichip Average (RMA) method and statistical analysis was performed using NIA Array Analysis (http://Igusun.grc.nia.nih.gov/ANOVA/).

2010-01-01 | E-GEOD-16007 | biostudies-arrayexpress

DNA methyltransferase 3b regulates articular cartilage homeostasis by altering chondrocyte metabolism

Project description:Osteoarthritis (OA) is the most common form of arthritis worldwide. It is a complex disease affecting the whole joint but is generally characterized by progressive degradation of articular cartilage. Recent genome-wide association screens have implicated distinct DNA methylation signatures in OA patients. We show that the de novo DNA methyltransferase (Dnmt) 3b, but not Dnmt3a, is present in healthy murine and human articular chondrocytes and expression decreases in OA mouse models and in chondrocytes from human OA patients. Targeted deletion of Dnmt3b in murine articular chondrocytes results in an early onset and progressive post-natal OA-like pathology. RNA-seq and MethylC-seq analyses of Dnmt3b loss-of-function chondrocytes shows that cellular metabolic processes are affected. Specifically, TCA metabolites and mitochondrial respiration are elevated. Importantly, a chondroprotective effect was found following Dnmt3b gain-of-function in murine articular chondrocytes in vitro and in vivo. This study shows that Dnmt3b plays a significant role in regulating post-natal articular cartilage homeostasis. Cellular pathways regulated by Dnmt3b in chondrocytes may provide novel targets for therapeutic approaches to treat OA.

2017-07-24 | GSE85148 | GEO

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