Dynamic transcriptome changes during adipose tissue energy expenditure reveal critical roles for long noncoding RNA regulators

Bai, Zhiqiang; Chai, Xiaoran; Yoon, Myeong Jin; Kim, Hye-Jin; Lo, Kinyui Alice; Zhang, Zhichun; Xu, Dan; Siang, Diana Teh Chee; Walet, Arcinas Camille Esther; Xu, Shaohai; Chia, Sook-Yoong; Chen, Peng; Yang, Hongyuan; Ghosh, Sujoy; Sun, Li

doi:10.1371/journal.pbio.2002176

Cited by 79 publications

(104 citation statements)

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“…First, HuR might target distinct sets of transcripts in different depots. This is consistent with the readily detectable depot-specific transcriptome signature 35,36 . Second, HuR might target similar transcripts in different depots and have similar effects on these targets, but each depot may elicit a depot-specific response program in different depots.…”

Section: Discussionsupporting

confidence: 86%

The RNA-binding protein HuR is a negative regulator in adipogenesis

et al. 2020

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Human antigen R (HuR) is an essential regulator of RNA metabolism, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in adipose tissues, accompanied by a systemic glucose intolerance and insulin resistance. HuR knockout also results in depot-specific phenotypes: it can repress myogenesis program in brown fat, enhance inflammation program in epidydimal white fat and induce browning program in inguinal white fat. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts including Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as an important posttranscriptional regulator of adipogenesis and provides insights into how RNA processing contributes to adipocyte development.

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Section: Discussionsupporting

confidence: 86%

The RNA-binding protein HuR is a negative regulator in adipogenesis

et al. 2020

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“…Mechanistically, Tug1 binds to an upstream PGC-1α enhancer element to enhance Ppargc1a promoter activity. In addition, a brown adipose tissue-enriched lncRNA, lncBATE10, functions as a decoy for repressor of PGC-1α, CUGBP Elav-Like Family Member 1 (Celf1), thereby protecting PGC-1α mRNA from repression by Celf1 [104]. However, the role and function of lncBATE10 in regulating the PGC-1α expression and fat browning during aging remains to be investigated.…”

Section: Pgc-1αmentioning

confidence: 99%

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

Lin

Kerkelä

2020

IJMS

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Aging is a major risk factor for cardiovascular diseases (CVDs), the major cause of death worldwide. Cardiac myocytes, which hold the most abundant mitochondrial population, are terminally differentiated cells with diminished regenerative capacity in the adult. Cardiomyocyte mitochondrial dysfunction is a characteristic feature of the aging heart and one out of the nine features of cellular aging. Aging and cardiac pathologies are also associated with increased senescence in the heart. However, the cause and consequences of cardiac senescence during aging or in cardiac pathologies are mostly unrecognized. Further, despite recent advancement in anti-senescence therapy, the targeted cell type and the effect on cardiac structure and function have been largely overlooked. The unique cellular composition of the heart, and especially the functional properties of cardiomyocytes, need to be considered when designing therapeutics to target cardiac aging. Here we review recent findings regarding key factors regulating cell senescence, mitochondrial health as well as cardiomyocyte rejuvenation.

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“…GUGBP Elav-like family member 1 (CELF1) is a RNA-binding protein which participates in mRNA targeting [31,32] and degradation [33]. It is involved in energy homeostasis transition in adipose tissue [34]. Controls alternative splicing in human cells [35].…”

Section: Resultsmentioning

confidence: 99%

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2017

Biopolym. Cell

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To identify novel protein partners of translation factor eEF1Bβ in nucleus of human lung carcinoma cells. Methods. Protein partners of eEF1Bβ in the nuclear fraction of A549 cells were identified by co-immunoprecipitation (co-IP) combined with liquid chromatographytandem mass spectrometry (LC-MS/MS). Specific protein partners of eEF1Bβ were further selected by using the results of previously published global, quantitative and dynamic mapping of protein subcellular localization with help of "Mapofthecell" program. Results. 104 highscored proteins interacting with eEF1Bβ in the nuclear fraction of A549 cells have been identified by mass-spectrometry. Among these proteins, 9 partners of eEF1Bβ were confirmed by the co-fractionation approach. Functional analysis of the partners has divided them on the pro-oncogenic (lung-cancer related) and neutral/anti-oncogenic moieties. These two groups are estimated to be spatially separated in human cancer cells. Conclusions. The position of eEF1Bβ as a link between the oncogenic and neutral/tumor-suppressor moieties of its protein partners in nucleus of lung cancer cells is suggested. Deciphering of a possible role of the eEF1Bβ distribution between the pro-cancer or anti-cancer communities of its protein partners can be a subject of further research.

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Dynamic transcriptome changes during adipose tissue energy expenditure reveal critical roles for long noncoding RNA regulators

Cited by 79 publications

References 52 publications

The RNA-binding protein HuR is a negative regulator in adipogenesis

The RNA-binding protein HuR is a negative regulator in adipogenesis

Regulatory Mechanisms of Mitochondrial Function and Cardiac Aging

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