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Linc-ADAIN, A Human Adipose LincRNA Regulates Adipogenesis by Modulating KLF5 and IL-8 mRNA stability

ABSTRACT: Linc-ADAIN, A Human Adipose LincRNA Regulates Adipogenesis by Modulating KLF5 and IL-8 mRNA stability

PROVIDER: PRJNA1099609 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28641927_1.fastq.gz	Fastqsanger.gz
	SRR28641927_2.fastq.gz	Fastqsanger.gz
	SRR28641928_1.fastq.gz	Fastqsanger.gz
	SRR28641928_2.fastq.gz	Fastqsanger.gz
	SRR28641929_1.fastq.gz	Fastqsanger.gz

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Linc-ADAIN, A Human Adipose LincRNA Regulates Adipogenesis by Modulating KLF5 and IL-8 mRNA stability

Project description:Adipose tissue remodeling and dysfunction, characterized by increased inflammation and insulin resistance, play a central role in obesity-related development of type 2 diabetes (T2DM) and cardiovascular diseases. Long intergenic non-coding RNAs (lincRNAs) are important regulators of cellular functions. Here we describe the functions of linc-ADAIN (ADipose Anti-INflammatory), an adipose lincRNA that is downregulated in white adipose tissue of obese humans. We demonstrate that linc-ADAIN knockdown (KD) increases KLF5 and IL-8 mRNA stability and translation, by interacting with IGF2BP2. Upregulation of KLF5 and IL-8, via linc-ADAIN KD, led to an enhanced adipogenic program and adipose tissue inflammation, mirroring the obese state, in vitro and in vivo, KD of linc-ADAIN in human ASC hTERT adipocytes implanted into mice, increased adipocyte size and macrophage infiltration compared to implanted control adipocytes, mimicking hallmark features of obesity-induced adipose tissue remodeling. Linc-ADAIN is an anti-inflammatory lincRNA that limits adipose tissue expansion and lipid storage.

2024-04-16 | GSE263852 | GEO

linc-ADAIN, a human adipose lincRNA, regulates adipogenesis by modulating KLF5 and IL-8 mRNA stability.

Project description:Adipose tissue remodeling and dysfunction, characterized by elevated inflammation and insulin resistance, play a central role in obesity-related development of type 2 diabetes (T2D) and cardiovascular diseases. Long intergenic non-coding RNAs (lincRNAs) are important regulators of cellular functions. Here, we describe the functions of linc-ADAIN (adipose anti-inflammatory), an adipose lincRNA that is downregulated in white adipose tissue of obese humans. We demonstrate that linc-ADAIN knockdown (KD) increases KLF5 and interleukin-8 (IL-8) mRNA stability and translation by interacting with IGF2BP2. Upregulation of KLF5 and IL-8, via linc-ADAIN KD, leads to an enhanced adipogenic program and adipose tissue inflammation, mirroring the obese state, in vitro and in vivo. KD of linc-ADAIN in human adipose stromal cell (ASC) hTERT adipocytes implanted into mice increases adipocyte size and macrophage infiltration compared to implanted control adipocytes, mimicking hallmark features of obesity-induced adipose tissue remodeling. linc-ADAIN is an anti-inflammatory lincRNA that limits adipose tissue expansion and lipid storage.

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Trans-chromosomal regulation by a novel lincRNA required for adipogenesis that escapes X-chromosome inactivation

Project description:Long noncoding RNAs (lncRNAs) have emerged as an important layer of genome regulation with common mechanistic themes including the formation of ribonucleoprotein complexes. Here, we present a novel X-linked lncRNA termed linc-Firre that escapes X-chromosome inactivation and forms trans-chromosomal interactions required for adipogenesis. Linc-Firre is exclusively nuclear and forms punctate expression foci on chromatin near its site of transcription on both X-chromosomes in human and mouse. Both the localization of linc-Firre and the association with the nuclear matrix protein hnRNPU require a conserved repeating RNA domain, R2D2. Collectively, these results reveal a lincRNA that escapes X-chromosome inactivation with a critical role in driving cell fate decisions by trans-chromosomal interactions. Replicate RNA-Seq analyses of oligo-mediated knockdowns of linc-FIRRE and hnRNPU in two different cellular contexts; HeLa cells and mouse embryonic stem cells.

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Transcriptome Analysis Identifies Linc-Yy1, A Novel Functional LincRNA During Myogenesis

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Linc-ADAIN Pulldown assay in Human Adipocytes.

Project description:Description: a biotinylated pulldown assay of linc-ADAIN, lincRNA vs Antisense Linc-ADAIN in primary human ASC adipocytes coupled to mass spectrometry (MS).

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RNA-Seq characterization of select lincRNA knockout mouse models

Project description:It has become clear that long intergenic noncoding RNAs (lincRNAs) are an important layer of genome regulation. Thousands have been identified in mammals, yet only a few have been tested through genetic ablation in animal models. Of the few that have, many yields weak to unobservable phenotypes, raising the question of their in vivo relevance. To more broadly investigate the functional relevance of lincRNAs in physiological conditions, we developed a collection of 18 lincRNA knockout strains. We found that two knockout strains, linc-Sox2 and linc-Foxf1a (Fendrr), exhibit perinatal lethal phenotypes in addition to multiple developmental abnormalities. Notably, in depth analysis of a third mutant strain, linc-Brn1b-/-, revealed defects in brain development, with distinct abnormalities in class-specific generation of upper layer II/III-IV neurons in the neocortex. Thus far, we found at least 6 of 18 mutant strains exhibit distinct developmental or lethality phenotypes. Therefore, this study demonstrates that lincRNAs are required for life and play critical roles during mammalian development, highlighting the importance of studying them further to better understand the molecular mechanisms leading to disease. Minimum 2 replicates each of select wild type and lincRNA knockout embryonic and postnatal tissues for three distinct lincRNA knockout mouse strains.

2013-11-30 | E-GEOD-49581 | biostudies-arrayexpress

Human Long Intergenic Noncoding RNA Linc-ADAL Knockdown in Mature Adipocytes using Lentiviral ShRNA

Project description:Thousands of human long intergenic noncoding RNAs (lincRNAs) have been detected in human adipose tissue. Here we characterized the function of one human adipse lincRNA, linc-ADAL (chr5:115292235-115296985) in mature adipcoytes through loss-of-function studies. Our results indicate that knockdown of linc-ADAL in differentiated adipocytes modulated expression of lipid metabolism genes.

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RNA-Seq characterization of select lincRNA knockout mouse models

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Control and Linc-AAM (a lincRNA associated with activated macrophages) knockdown RAW264.7 cells expression profiling under AEPS (the polysaccharide from the roots of Actinidia eriantha) stimulation

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