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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

ABSTRACT: RNA immunoprecipitation sequencing (RIP seq) using PTBP1 antibody to identify the potential targets of in DCRT-KO and WT cell

ORGANISM(S): Homo sapiens

PROVIDER: GSE243739 | GEO | 2023/09/30

REPOSITORIES: GEO

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

Project description:LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (RIP-seq)

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1

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LncRNA DCRT protects against dilated cardiomyopathy via binding to PTBP1 (Iso-seq)

Project description:Dilated cardiomyopathy (DCM) is characterized by left ventricular dilation and continuous systolic dysfunction. Mitochondrial impairment is critical in DCM, but the mechanism remains to be elucidated. Here we explored the cardio-protective role of a heart-enriched long non-coding RNA (lncRNA), named dilated cardiomyopathy repressive transcript (DCRT), via maintaining mitochondrial function. We found the lncRNA DCRT was highly enriched in normal heart tissue and its expression was significantly down-regulated in myocardium of DCM patients. DCRT knockout in mice spontaneously developed cardiac dysfunction with cardiac enlargement and mitochondrial impairment. DCRT transgenic or overexpressed mice attenuated cardiac dysfunction induced by transverse aortic constriction (TAC) treatment.

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RIP-seq analysis of PTBP1-bound RNAs

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Project description:We identify a lncRNA which low expresses and regulates self-renewal of bladder cancer stem cell. So we named it lncRNA-LBCS (low expresses in bladder cancer stem cell). Further study finds that lncRNA-LBCS bind to hnRNPK and PTBP1. To investigate the genes regulated by these, we knockdown lncRNA-LBCS, hnRNPK and PTBP1 by siRNA, respectively, and perform high-throughput sequence. So we identify a series of genes regulated by lncRNA-LBCS, hnRNPK and PTBP1, respectively.

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iiCLIP protocol benchmarking with PTBP1

Project description:We describe an improved individual nucleotide resolution CLIP protocol (iiCLIP), which can be completed within 4 days from UV crosslinking to libraries for sequencing. For benchmarking, we directly compared PTBP1 iiCLIP libraries with the iCLIP2 protocol produced under standardised conditions with 1 million HEK293 cells, and with public eCLIP and iCLIP PTBP1 data. There are 3 PTBP1 iiCLIP libraries, 1 input iiCLIP library and 1 PTBP1 iCLIP2 library produced in this study.

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Proteome changes in PTBP1 deficient hematopoietic cells

Project description:Ribosomopathies constitute a range of disabling conditions associated with defective protein synthesis mainly affecting hematopoietic stem cells (HSCs) and erythroid development. Here we demonstrate that deletion of Polypyrimidine Tract Binding Protein 1 (PTBP1) in the hematopoietic compartment led to the development of a ribosomopathy-like condition. Specifically, loss of PTBP1 was associated with a decrease in HSC self-renewal, erythroid differentiation and protein synthesis. Consistent with its function as a splicing regulator, PTBP1 deficiency led to splicing defects in hundreds of genes and we demonstrate that the up-regulation of a specific isoform of CDC42 could partly mimic the protein synthesis defect associated with loss of PTBP1. Furthermore, PTBP1 deficiency was associated with a marked defect in ribosome biogenesis and a selective reduction in the translation of mRNAs encoding ribosomal proteins. Collectively, this work identifies PTBP1 as a key integrator of ribosomal functions and highlights the broad functional repertoire of RNA binding proteins.

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Dhcr24 activates the PI3K/Akt/HKII pathway and protects against dilated cardiomyopathy in mice.

Project description:Background24-dehydrocholesterol reductase (Dhcr24) catalyzes the last step of cholesterol biosynthesis, which is required for normal development and anti-apoptotic activities of tissues. We found that Dhcr24 expression decreased in the cTnTR 141W dilated cardiomyopathy (DCM) transgenic mice. Therefore, we tested whether rescued expression of Dhcr24 could prevent the development of DCM and its possible mechanism.MethodsHeart tissue specific transgenic overexpression mice of Dhcr24 was generated, then was crossed to cTnTR 141W mouse to obtain the double transgenic mouse (DTG). The phenotypes were demonstrated by the survival, cardiac geometry and function analysis, as well as microstructural and ultrastructural observations based on echocardiography and histology examination. The pathway and apoptosis were analysed by western blotting and TUNEL assay in vivo and in vitro.ResultsWe find that Dhcr24 decreased in hearts tissues of cTnTR 141W and LMNAE 82K DCM mice. The transgenic overexpression of Dhcr24 significantly improves DCM phenotypes in cTnTR 141W mice, and activates PI3K/Akt/HKII pathway, followed by a reduction of the translocation of Bax and release of cytochrome c, caspase-9 and caspase-3 activation and myocyte apoptosis. Knockdown the expression of Dhcr24 reduces the activation of PI3K/Akt/HKII pathway and inhibition of the mitochondrial-dependent apoptosis. The anti-apoptotic effect of Dhcr24 could be completely removed by the inhibition of PI3K pathway and partly removed by the HKII inhibitor in H9c2 cell line.ConclusionCompensatory expression of Dhcr24 protect against DCM through activated PI3K/Akt/HKII pathway and reduce Bax translocation. This is the first investigation for the molecular mechanism of Dhcr24 participate in development of DCM.

| S-EPMC6354314 | biostudies-literature

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