De Novo Reconstruction of Adipose Tissue Transcriptomes Reveals Long Non-coding RNA Regulators of Brown Adipocyte Development

Alvarez-Dominguez, Juan R.; Bai, Zhiqiang; Xu, Dan; Yuan, Bingbing; Lo, Kinyui Alice; Yoon, Myeong Jin; Lim, Yen Ching; Knoll, Marko; Slavov, Nikolai; Chen, Shuai; Chen, Peng; Lodish, Harvey F.; Sun, Li

doi:10.1016/j.cmet.2015.04.003

Cited by 178 publications

(231 citation statements)

References 51 publications

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“…lnc-BATE1 inhibition in brown preadipocytes resulted in decreased expression of brown fat markers (such as UCP1, PRDM16, and PGC1α), mitochondrial markers and, to a lesser extent, common adipogenic markers (PPARγ, CEBPα, FABP4, and AdipoQ), with limited effects on lipid accumulation and cell morphology; similar effects of lnc-BATE1 knockdown in beige adipocytes were also found [51]. Moreover, depletion of lnc-BATE1 in mouse mature brown adipocytes reduced BAT, mitochondrial, and common adipogenic markers, indicating lnc-BATE1 was essential for development and maintenance of mature brown adipocytes [51]. Indeed, lnc-BATE1 acts in trans to selectively sustain the core BAT gene program and repress WAT-selective genes through binding hnRNP-U, and both lnc-BATE1 and hnRNP-U were required for brown adipogenesis [51].…”

Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 92%

“…A recent study found that lnc-BATE1 was dramatically upregulated during brown adipogenesis or cold-induced beige adipocyte expansion [51]. lnc-BATE1 inhibition in brown preadipocytes resulted in decreased expression of brown fat markers (such as UCP1, PRDM16, and PGC1α), mitochondrial markers and, to a lesser extent, common adipogenic markers (PPARγ, CEBPα, FABP4, and AdipoQ), with limited effects on lipid accumulation and cell morphology; similar effects of lnc-BATE1 knockdown in beige adipocytes were also found [51]. Moreover, depletion of lnc-BATE1 in mouse mature brown adipocytes reduced BAT, mitochondrial, and common adipogenic markers, indicating lnc-BATE1 was essential for development and maintenance of mature brown adipocytes [51].…”

Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 99%

“…Moreover, depletion of lnc-BATE1 in mouse mature brown adipocytes reduced BAT, mitochondrial, and common adipogenic markers, indicating lnc-BATE1 was essential for development and maintenance of mature brown adipocytes [51]. Indeed, lnc-BATE1 acts in trans to selectively sustain the core BAT gene program and repress WAT-selective genes through binding hnRNP-U, and both lnc-BATE1 and hnRNP-U were required for brown adipogenesis [51]. These data demonstrate that lnc-BATE1 is an essential factor during brown adipogenesis for induction of multiple mitochondrial proteins and for thermogenesis in brown adipocytes.…”

Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 99%

“…Followed to SRA, lnc-RAP-n, slincRAD, PU.1 AS, HOTAIR, ADINR, and NEAT1 are also found to be involved in white preadipocyte differentiation [13, 34, 42, 45, 46, 50]. Furthermore, Blnc1 and lnc-BATE-1 positively regulate brown or beige adipogenesis via forming a ribonucleoprotein complex with distinct transcriptional factors [33, 51]. …”

Section: Clinical Significance Of Lncrnas For Fighting Against Obesitymentioning

confidence: 99%

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Long noncoding RNAs in regulating adipogenesis: new RNAs shed lights on obesity

Wei

Jiang

et al. 2016

Cell. Mol. Life Sci.

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Long noncoding RNAs (lncRNAs) are an emerging class of regulators involved in a myriad of biological processes. Recent studies have revealed that many lncRNAs play pivotal roles in regulating adipocyte development. Due to the prevalence of obesity and the serious effects of adiposity on human health and society development, it is necessary to summarize functions and recent advances of lncRNAs in adipogenesis. In this review, we highlight functional lncRNAs contributed to the regulation of adipogenesis, discussing their potential use as therapeutic targets to combat human obesity.

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Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 92%

Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 99%

Section: Lncrnas In Brown/beige Adipocyte Developmentmentioning

confidence: 99%

Section: Clinical Significance Of Lncrnas For Fighting Against Obesitymentioning

confidence: 99%

See 2 more Smart Citations

Long noncoding RNAs in regulating adipogenesis: new RNAs shed lights on obesity

Wei

Jiang

et al. 2016

Cell. Mol. Life Sci.

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“…Long noncoding RNAs (lncRNAs) are non-protein-coding transcripts longer than 200 nucleotides [6] that were previously considered “transcription noise”, but studies have increasingly demonstrated that lncRNA transcripts are widely involved in almost every aspect of cellular biological functions, such as cell proliferation [7, 8], differentiation [9, 10], metabolism [11], and apoptosis [12]. Accumulating evidence suggests that the aberrant expression of lncRNAs plays an important role in the regulation of pancreatic β-cell function.…”

Section: Introductionmentioning

confidence: 99%

Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet β-Cell Function

Ruan¹,

Lin²,

Ma³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The islet is an important endocrine organ to secrete insulin to regulate the metabolism of glucose and maintain the stability of blood glucose. Long noncoding RNAs (lncRNAs) are involved in a variety of biological functions and play key roles in many diseases, including type 2 diabetes (T2D). The aim of this study was to determine whether lncRNA-p3134 is associated with glucose metabolism and insulin signaling in pancreatic β cells. Methods: LncRNA microarray technology was used to identify the differentially expressed circulating lncRNAs in T2D patients. RT-PCR analyses were performed to determine the expression of lncRNA-p3134 in 30 pairs of diabetic and non-diabetic patients. The correlation of lncRNA-p3134 to clinical data from T2D patients was analyzed. LncRNA-p3134 was overexpressed in Min6 cells and db/db mice by adenovirus-mediated technology. CCK-8, TUNEL, Western blot, glucose-stimulated insulin secretion (GSIS), ELISAs and immunochemistry were performed to determine the effect of lncRNA-p3134 on proliferation, apoptosis and insulin secretion both in vitro and vivo. Results: The circulating level of lncRNA-p3134 was higher in diabetic patients than in non-diabetic controls and was correlated with fasting blood glucose and HOMA-β levels. The lncRNA-p3134 had risen by 4 times in serum exosomes but nearly unchanged in exosome-free samples. The secretion of lncRNA-p3134 was dynamically modulated by glucose in both Min6 cells and isolated mouse islet cells. LncRNA-p3134 positively regulate GSIS through promoting of key regulators (Pdx-1, MafA, GLUT2 and Tcf7l2) in β cells. In addition, the overexpression of lncRNA-p3134 resulted in a decreased apoptosis ratio and partially reversed the glucotoxicity effects on GSIS function in Min6 cells. The restoration of insulin synthesis and secretion the increase of the insulin positive cells areas by upregulation of lncRNA-p3134 in db/db mice confirmed the compensatory role of lncRNA-p3134 to preserve β-cell function. Furthermore, a protective effect of lncRNA-p3134 on GSIS by positive modulation of PI3K/Akt/mTOR signaling was also confirmed. After blocking the PI3K/AKT signals with their specific inhibitor, the effect of overexpressed lncRNA-p3134 on insulin secretion was obviously attenuated. Conclusion: Taken together, the results of this study provide new insights into lncRNA-p3134 regulation in pancreatic β cells and provide a better understanding of novel mechanism of glucose homeostasis.

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Long noncoding RNAs in cardiometabolic disorders

et al. 2022

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The advancement of medical technology has led not only to an increase in life expectancy but also to a rise in aging‐related diseases. Aging promotes metabolic disorders, in turn affecting cardiovascular health. Derailment of biological processes in the pancreas, liver, adipose tissue, and skeletal muscle impairs glucose and lipid metabolism, and mitochondrial function, triggering the development of diabetes and lipid‐related disorders that inflict damage on cardiac and vascular tissues. Long noncoding RNAs (lncRNAs) regulate a wide range of biological process and are one of the key factors controlling metabolism and mitochondria. Here, we discuss the versatile function of lncRNAs involved in the metabolic regulation of glucose and lipid, and mitochondrial function, and how the dysregulation of lncRNAs induces the development of various metabolic disorders and their cardiovascular consequences.

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De Novo Reconstruction of Adipose Tissue Transcriptomes Reveals Long Non-coding RNA Regulators of Brown Adipocyte Development

Cited by 178 publications

References 51 publications

Long noncoding RNAs in regulating adipogenesis: new RNAs shed lights on obesity

Long noncoding RNAs in regulating adipogenesis: new RNAs shed lights on obesity

Circulating LncRNAs Analysis in Patients with Type 2 Diabetes Reveals Novel Genes Influencing Glucose Metabolism and Islet β-Cell Function

Long noncoding RNAs in cardiometabolic disorders

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