Functional consequences of impaired linc-GALNTL6-4 in adipocytes
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ABSTRACT:
PROVIDER: PRJNA906089 | ENA |
REPOSITORIES: ENA
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Project description:The relevance of adipose-derived long noncoding RNAs (lncRNAs) to the regulation of gene expression patterns related to the obese phenotype remains elusive. Here, the analysis of transcriptomes of adipose tissue before-after significant weight loss led to the identification of 496 putative lncRNAs (FDR p-values <0.05). Only the nonconserved linc-GALNTL6-4 displayed a fold-change above 2 plus adjusted p-value <0.0001. Exploration of additional omental and subcutaneous fat samples confirmed diminished linc-GALNTL6-4 in obese subjects, while lncRNA-mRNA co-expression analyses highlighted its association with fatty acid metabolism. Concurrently, the expression of this unique lncRNA towered in ex vivo isolated and in vitro differentiated adipocytes, being compromised under conditions that mimicked inflammation in obese adipocytes. On the other hand, the knockdown of linc-GALNTL6-4 in fat cell progenitors conveys impaired differentiation, fostering deranged expression patterns in differentiated adipocytes, including the increased expression of genes devoted to the transport of lipids, such as Apolipoprotein C1 (APOC1) and the intracellular fatty acid-binding protein FABP3. Conversely, overexpression of linc-GALNTL6-4 ameliorated adipocyte performance through the specific control of the short-chain fatty acid receptor FFAR3. Current data unveil the unforeseen relevance of linc-GALNTL6-4 as a modulator of fatty acid sensing in adipocytes deeply challenged by body weight and meta-inflammation.
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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.
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Project description:The relevance of adipose-derived long noncoding RNAs (lncRNAs) to the regulation of gene expression patterns related to the obese phenotype remains elusive. Here, the analysis of transcriptomes of adipose tissue before-after significant weight loss led to the identification of 496 putative lncRNAs (FDR p-values <0.05). Only the nonconserved linc-GALNTL6-4 displayed a fold-change above 2 plus adjusted p-value <0.0001. Exploration of additional omental and subcutaneous fat samples confirmed diminished linc-GALNTL6-4 in obese subjects, while lncRNA-mRNA co-expression analyses highlighted its association with fatty acid metabolism. Concurrently, the expression of this unique lncRNA towered in ex vivo isolated and in vitro differentiated adipocytes, being compromised under conditions that mimicked inflammation in obese adipocytes. On the other hand, the knockdown of linc-GALNTL6-4 in fat cell progenitors conveys impaired differentiation, fostering deranged expression patterns in differentiated adipocytes, including the increased expression of genes devoted to the transport of lipids, such as Apolipoprotein C1 (APOC1) and the intracellular fatty acid-binding protein FABP3. Conversely, overexpression of linc-GALNTL6-4 ameliorated adipocyte performance through the specific control of the short-chain fatty acid receptor FFAR3. Current data unveil the unforeseen relevance of linc-GALNTL6-4 as a modulator of fatty acid sensing in adipocytes deeply challenged by body weight and meta-inflammation.
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