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MiR-146a regulates many lncRNAs in RAS induced senescence [Anti-146a]

ABSTRACT: miR-146a is a known anti-inflammatory miRNA. Intringuigly, it is overexpressed in RAS-induced senescent cells which is accompanied with a rich pro-inflammatoy secretpry phenotype. We aim to study possible sponges for miR-146a.

ORGANISM(S): Homo sapiens

PROVIDER: GSE150325 | GEO | 2021/05/11

REPOSITORIES: GEO

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miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP]

Project description:miR-146a is a known anti-inflammatory miRNA. Intringuigly, it is overexpressed in RAS-induced senescent cells which is accompanied with a rich pro-inflammatoy secretpry phenotype. We aim to study possible sponges for miR-146a.

2021-05-11 | GSE150324 | GEO

miR-146a regulates many lncRNAs in RAS induced senescence [Anti-146a]

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miR-146a regulates many lncRNAs in RAS induced senescence [miR-CLIP

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

2021-05-11 | GSE150326 | GEO

Data in support of Absence of miRNA-146a differentially alters microglia function and proteome

Project description:MiR-146a is an important regulator of innate inflammatory responses and is also implicated in cell death and survival. Here, we identified microglia as the main cellular source of miR-146a among mouse CNS resident cells. We further characterized the phenotype of miR-146a KO microglia cells during in vivo demyelination induced by cuprizone (CPZ) and found reduced number of CD11c+ microglia in the KO compared to WT mice. Microglia were also isolated from the brain, and the proteome was analyzed by liquid chromatography mass spectrometry.

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Mir-146a wild-type 3ʹ sequence identity is dispensable for proper innate immune function in vivo

Project description:A long-prevailing model has held that the “seed” region (nucleotides 2-8) of a microRNA is typically sufficient to mediate target recognition and repression. However, numerous recent studies, both within the context of defining miRNA/target pairs by direct physical association and by directly assessing this model in vivo in C. elegans have brought this model into question. To test the importance of miRNA 3' pairing in vivo, in a mammalian system, we engineered a mutant murine mir-146a allele in which the 5' half of the mature microRNA retains the sequence of the wild-type mir-146a but the 3ʹ half has been altered to be anti-complementary to the wild-type miR-146a sequence. Mice homozygous or hemizygous for this mutant allele are phenotypically indistinguishable from wild-type controls and do not recapitulate any of the immunopathology previously described for mir-146a-null mice. Our results strongly support the conclusion that 3ʹ pairing is dispensable in the context of the function of a key mammalian microRNA.

2019-02-09 | PXD011413 | Pride

Circular RNA circGNAQ acts as the sponge of miR-146a-5p to delay endothelial cell senescence and atherosclerosis progression

Project description:Endothelial cell senescence is one of the most important causes of vascular dysfunction and atherosclerosis. Circular RNAs (circRNAs) are endogenous RNA molecules with covalently closed-loop structures, which have been reported to be abnormally expressed in many human diseases. However, the potential role of circRNAs in endothelial cell senescence remains unknown. Here, we compared the expression patterns of circRNAs in young and senescent human endothelial cells using RNA sequencing. Among the differentially expressed endothelial cell senescence-associated circRNAs, we identified circGNAQ, generated by circularization of exons 4 and 5 of the GNAQ gene, as a circRNA showing markedly reduced levels in senescent endothelial cells. CircGNAQ silencing in young endothelial cells triggered senescence, as determined by a rise in senescence-associated β-galactosidase activity, reduced cell proliferation, and suppressed angiogenesis; circGNAQ overexpression showed the opposite effects. Mechanistic studies revealed that circGNAQ acted as an endogenous miR-146a-5p sponge to sequester and inhibit miR-146a-5p activity, leading to increased PLK2 expression. In vivo studies showed that circGNAQ overexpression delayed endothelial cell senescence and atherosclerosis progression in ApoE-/- mice. These results revealed an important role for circGNAQ in cellular senescence and provide novel insight into the role of circRNAs in atherosclerosis progression.

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Global transcriptome profiling was performed for keratinocytes transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC).

Project description:To find out potiential target gene of miR-146a,we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to target miR-146a. Human keratinocytes was transfected with either miR-146a mimics (Pre-146a) or negative control (Pre-NC) for 48h, then RNA was extracted for whole genome microarray expression profiling.

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MicroRNA-146a modulates B-cell oncogenesis by regulating EGR1

Project description:miR-146a is a NF-κB induced microRNA that serves as a feedback regulator of this critical pathway. In mice, deficiency of miR-146a results in hematolymphoid cancer at advanced ages as a consequence of constitutive NF-κB activity. In this study, we queried whether the deficiency of miR-146a contributes to B-cell oncogenesis. Combining miR-146a deficiency with transgenic expression of c-Myc led to the development of highly aggressive B-cell malignancies. Mice transgenic for c-Myc and deficient for miR-146a were characterized by significantly shortened survival, increased lymph node involvement, differential involvement of the spleen and a mature B-cell phenotype. High-throughput sequencing of the tumors revealed significant dysregulation of approximately 250 genes. Amongst these, the transcription factor Egr1 was consistently upregulated in mice deficient for miR-146a. Interestingly, transcriptional targets of Egr1 were enriched in both the high-throughput dataset and in a larger set of miR-146a-deficient tumors. miR-146a overexpression led to downregulation of Egr1 and downstream targets with concomitant decrease in cell growth. Direct targeting of the human EGR1 by miR-146a was seen by luciferase assay. Together our findings illuminate a bona fide role for miR-146a in the modulation of B-cell oncogenesis and reveal the importance of understanding microRNA function in a cell- and disease-specific context.

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