Airn isoforms are important for the functions of cardiomyocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA343927 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To elucidate the function of Airn isoforms in the heart, we conducted loss-of-function experiments in murine cardiomoycyte cell line HL-1.
2018-02-28 | GSE87222 | GEO
Project description:To elucidate the function of Airn isoforms in the heart, we conducted RNA immunoprecipitation experiment followed by microarray (RIP-chip) in murine cardiomoycyte cell line HL-1.
2018-02-28 | GSE87221 | GEO
Project description:Airn isoforms are important for the functions of cardiomyocytes (Gene_Array-Airn)
| PRJNA343929 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-02-28 | GSE87223 | GEO
Project description:Airn isoforms are important for the functions of cardiomyocytes (RIP-chip-Igf2bp2)
| PRJNA343931 | ENA
Project description:To test if the imprinted long non-coding RNA (lncRNA) Airn transcription or its product silences the protein-coding Igf2r gene, we shortened the endogenous lncRNA to four different lengths by inserting polyadenylation (polyA) cassettes on the paternal chromosome via homologous recombination in ES cells. ES cell differentiation was used to recapitulate the developmental onset of Airn and Igf2r imprinted expression and polyA cassettes inserted before (T3, T16, T27) or after (T31, T51) the Igf2r promoter successfully truncated Airn, with the exception of T27. RNA hybridization to a tiling array (MIRTA) demonstrated loss of Airn upstream of the Igf2r promoter (except T27) and absence of novel spliced variants in all truncation alleles. To further test the transcriptional overlap model we moved the Airn promoter ~700bp before the Igf2r TSS in ES cells that lack an endogenous paternal Airn promoter and called this cell line FAP (Forward-Airn-Promoter). RNA hybridization to a tiling array (MIRTA) demonstrated that the moved Airn promoter expresses Airn in wildtype orientation and terminates at the wildtype 3' end. ES cell lines expressing different Airn variants were differentiated on gelatinized dishes after feeder cell depletion and LIF withdrawal by 0.27M-BM-5M retinoic acid for 5 days and Airn length was assayed.
2012-12-20 | E-GEOD-41444 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) have emerged as important regulators in a variety of human diseases. It has been suggested that dysregulation of liver sinusoidal endothelial cells (LSECs) phenotype is a critical early event in the fibrotic process. However, the biological function of lncRNAs in LSECs still remains unclear. Here, we identified that lncRNA-Airn was significantly up-regulated in liver tissues and LSECs of CCl4-induced liver fibrosis. Moreover, the expression of AIRN in human cirrhotic liver tissues and serums was remarkably increased as compared with healthy controls. In vivo studies showed that Airn deficiency aggravated CCl4- and BDL-induced liver fibrosis, while Airn overexpression by adeno-associated viral vector serotype 8 vector alleviated CCl4-induced liver fibrosis. Furthermore, we revealed that Airn maintained LSECs differentiation in vivo and in vitro. Additionally, Airn inhibited hepatic stellate cells (HSCs) activation indirectly by regulating LSECs differentiation and promoted hepatocytes (HCs) proliferation by the increased paracrine secretion of Wnt2a and HGF from LSECs. Mechanistically, our results demonstrated that Airn maintained LSECs differentiation through KLF2-endothelial nitric oxide synthase (eNOS)-soluble guanylate cyclase (sGC) pathway, thereby promoting HSCs quiescence and HCs proliferation. In conclusion, our work identified that Airn is beneficial to liver fibrosis by maintaining LSECs differentiation and might be a novel serum biomarker for liver fibrogenesis.
2021-05-11 | GSE174175 | GEO
Project description:Opposing functions of BRD4 isoforms in breast cancer
| PRJNA561383 | ENA
Project description:To test if the imprinted long non-coding RNA (lncRNA) Airn transcription or its product silences the protein-coding Igf2r gene, we shortened the endogenous lncRNA to four different lengths by inserting polyadenylation (polyA) cassettes on the paternal chromosome via homologous recombination in ES cells. ES cell differentiation was used to recapitulate the developmental onset of Airn and Igf2r imprinted expression and polyA cassettes inserted before (T3, T16, T27) or after (T31, T51) the Igf2r promoter successfully truncated Airn, with the exception of T27. RNA hybridization to a tiling array (MIRTA) demonstrated loss of Airn upstream of the Igf2r promoter (except T27) and absence of novel spliced variants in all truncation alleles. To further test the transcriptional overlap model we moved the Airn promoter ~700bp before the Igf2r TSS in ES cells that lack an endogenous paternal Airn promoter and called this cell line FAP (Forward-Airn-Promoter). RNA hybridization to a tiling array (MIRTA) demonstrated that the moved Airn promoter expresses Airn in wildtype orientation and terminates at the wildtype 3' end.
2012-12-20 | GSE41444 | GEO
Project description:RATIONALE:Increasing evidence indicates the presence of lncRNAs in various cell types. Airn is an imprinting gene transcribed from the paternal chromosome. It is in antisense orientation to the imprinted, but maternally derived, Igf2r gene, on which Airn exerts its regulation in cis. Although Airn is highly expressed in the heart, functions aside from imprinting remain unknown. OBJECTIVE:Here, we studied the functions of Airn in the heart, especially cardiomyocytes. METHODS AND RESULTS:Silencing of Airn via siRNAs augmented cell death, vulnerability to cellular stress, and reduced cell migration. To find the cause of such phenotypes, the potential binding partners of Airn were identified via RNA pull-down followed by mass spectrometry, which indicated Igf2bp2 (insulin-like growth factor 2 mRNA-binding protein 2) and Rpa1 (replication protein A1) as potential binding partners. Further experiments showed that Airn binds to Igf2bp2 to control the translation of several genes. Moreover, silencing of Airn caused less binding of Igf2bp2 to other mRNAs and reduced translation of Igf2bp2 protein. CONCLUSIONS:Our study uncovers a new function of Airn and demonstrates that Airn is important for the physiology of cardiomyocytes.
| S-EPMC5948151 | biostudies-literature