Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Ribosome profiling of chondrocytic cell line SW1353 following exposure to IL-1B

ABSTRACT: Osteoarthritis is a chronic disease characterised by the loss of articular cartilage in synovial joints through a process of extracellular matrix destruction that is strongly associated with inflammatory stimuli. Chondrocytes undergo changes to their protein translation capacity during osteoarthritis, but a study of how disease-relevant signals effect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study we describe how the inflammatory cytokine interleukin 1-beta (IL-1β) rapidly affects protein translation in the chondrocytic cell line SW1353. Using ribosome profiling we demonstrate that IL-1β induced altered translation of inflammatory-associated transcripts such as NFKB1, TNFAIP2, MMP13, CCL2 and CCL7, as well as a number of ribosome-associated transcripts, through differential translation and the use of multiple open reading frames. Proteomic analysis of the cellular layer and the conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. These translationally regulated secreted proteins included a number of chemokines and cytokines, underlining the rapid, translationally-mediated inflammatory cascade that is initiated by IL-1 β.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Homo sapiens

SUBMITTER: Ben McDermott

PROVIDER: E-MTAB-7466 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Translational regulation contributes to the secretory response of chondrocytic cells following exposure to interleukin-1β.

McDermott Benjamin T BT Peffers Mandy J MJ McDonagh Brian B Tew Simon R SR

The Journal of biological chemistry 20190712 35

Osteoarthritis is a chronic disease characterized by the loss of articular cartilage in synovial joints through a process of extracellular matrix destruction that is strongly associated with inflammatory stimuli. Chondrocytes undergo changes to their protein translational capacity during osteoarthritis, but a study of how disease-relevant signals affect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study, we describe how the inflammatory c ...[more]

PMID: 31300557

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Project description:The role of long noncoding RNA (lncRNA) in adult hearts is unknown; also unclear is how lncRNA modulates nucleosome remodelling. An estimated 70% of mouse genes undergo antisense transcription1, including myosin heavy chain 7 (Myh7), which encodes molecular motor proteins for heart contraction2. Here we identify a cluster of lncRNA transcripts from Myh7 loci and demonstrate a new lncRNA–chromatin mechanism for heart failure. In mice, these transcripts, which we named myosin heavy-chain-associated RNA transcripts (Mhrt), are cardiac-specific and abundant in adult hearts. Pathological stress activates the Brg1–Hdac–Parp chromatin repressor complex3 to inhibit Mhrt transcription in the heart. Such stress-induced Mhrt repression is essential for cardiomyopathy to develop: restoring Mhrt to the pre-stress level protects the heart from hypertrophy and failure. Mhrt antagonizes the function of Brg1, a chromatin-remodelling factor that is activated by stress to trigger aberrant gene expression and cardiac myopathy3. Mhrt prevents Brg1 from recognizing its genomic DNA targets, thus inhibiting chromatin targeting and gene regulation by Brg1. It does so by binding to the helicase domain of Brg1, a domain that is crucial for tethering Brg1 to chromatinized DNA targets. Brg1 helicase has dual nucleic-acid-binding specificities: it is capable of binding lncRNA (Mhrt) and chromatinized—but not naked—DNA. This dual-binding feature of helicase enables a competitive inhibition mechanism by which Mhrt sequesters Brg1 from its genomic DNA targets to prevent chromatin remodelling. A Mhrt–Brg1 feedback circuit is thus crucial for heart function. Human MHRT also originates from MYH7 loci and is repressed in various types of myopathic hearts, suggesting a conserved lncRNA mechanism in human cardiomyopathy. Our studies identify a cardioprotective lncRNA, define a new targeting mechanism for ATP-dependent chromatin-remodelling factors, and establish a new paradigm for lncRNA–chromatin interaction. Overexpression of murine non-coding RNAs in human cell line, comparison of RNA-sequencing with Ribosome Profiling

Dataset Information

Ribosome profiling of chondrocytic cell line SW1353 following exposure to IL-1B

Publications

Translational regulation contributes to the secretory response of chondrocytic cells following exposure to interleukin-1β.

Similar Datasets

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