A Liver-Enriched Long Non-Coding RNA, lncLSTR, Regulates Systemic Lipid Metabolism in Mice

Li, Ping; Ruan, Xiangbo; Yang, Ling; Kiesewetter, Kurtis; Zhao, Yi; Luo, Haitao; Chen, Yong; Guček, Marjan; Zhu, Jun; Cao, Haiming

doi:10.1016/j.cmet.2015.02.004

Cited by 258 publications

(229 citation statements)

References 43 publications

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“…injection (250-500 mg/kg) of tribromoethanol (Avertin). Primary hepatocytes were then isolated using a 2-step collagenase perfusion protocol (59). Hepatocytes (~0.7 × 10 6 cells/well) were cultured at 60% to 70% confluence in DMEM (4.5 g/l glucose) containing 10% FBS in collagen I-coated, 6-well plates (Corning).…”

Section: Discussionmentioning

confidence: 99%

Hepatic Gi signaling regulates whole-body glucose homeostasis

Rossi¹,

Zhu²,

McMillin³

et al. 2018

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

Hepatic Gi signaling regulates whole-body glucose homeostasis

Rossi¹,

Zhu²,

McMillin³

et al. 2018

Journal of Clinical Investigation

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“…After four washes with PBS-T, blots were incubated at room temperature for 1 hour with the fluorescenceconjugated secondary antibody (IRDye 800 CW donkey anti-goat; LI-COR), with 5.0 ml of secondary antibody diluted to 15 ml in LI-COR Blocking Buffer containing 150 ml of 20% Tween-20 and 30 ml of 10% SDS. Membranes were washed four times with PBS-T and twice with 1Â PBS, and the bound antibody was visualized using a quantitative fluorescence imaging system (LI-COR) (Li et al, 2015).…”

Section: Methodsmentioning

confidence: 99%

Creation of Apolipoprotein C-II (ApoC-II) Mutant Mice and Correction of Their Hypertriglyceridemia with an ApoC-II Mimetic Peptide

Sakurai¹,

Sakurai²,

Vaisman³

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Apolipoprotein C-II (apoC-II) is a cofactor for lipoprotein lipase, a plasma enzyme that hydrolyzes triglycerides (TGs). ApoC-II deficiency in humans results in hypertriglyceridemia. We used zinc finger nucleases to create Apoc2 mutant mice to investigate the use of C-II-a, a short apoC-II mimetic peptide, as a therapy for apoC-II deficiency. Mutant mice produced a form of apoC-II with an uncleaved signal peptide that preferentially binds high-density lipoproteins (HDLs) due to a 3-amino acid deletion at the signal peptide cleavage site. Homozygous Apoc2 mutant mice had increased plasma TG (757.5 6 281.2 mg/dl) and low HDL cholesterol (31.4 6 14.7 mg/dl) compared with wild-type mice (TG, 55.9 6 13.3 mg/dl; HDL cholesterol, 55.9 6 14.3 mg/dl). TGs were found in light (density , 1.063 g/ml) lipoproteins in the size range of verylow-density lipoprotein and chylomicron remnants (40-200 nm). Intravenous injection of C-II-a (0.2, 1, and 5 mmol/kg) reduced plasma TG in a dose-dependent manner, with a maximum decrease of 90% occurring 30 minutes after the high dose. Plasma TG did not return to baseline until 48 hours later. Similar results were found with subcutaneous or intramuscular injections. Plasma half-life of C-II-a is 1.33 6 0.72 hours, indicating that C-II-a only acutely activates lipolysis, and the sustained TG reduction is due to the relatively slow rate of new TG-rich lipoprotein synthesis. In summary, we describe a novel mouse model of apoC-II deficiency and show that an apoC-II mimetic peptide can reverse the hypertriglyceridemia in these mice, and thus could be a potential new therapy for apoC-II deficiency.

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“…In addition, SHP acts as a transcriptional repressor of microRNA expression and function through interaction with other nuclear receptors 49, 50, 51, 52. Accumulative evidence demonstrates the involvement of long noncoding RNAs (lncRNAs) in lipid metabolism, microbial susceptibility, nuclear reprogramming, and epigenetics 53, 54…”

Section: Nuclear Receptor Crosstalk With Noncoding Rnasmentioning

confidence: 99%

Nuclear receptors and liver disease: Summary of the 2017 basic research symposium

Tran

Liu

Huang

et al. 2018

Hepatology Communications

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The nuclear receptor superfamily contains important transcriptional regulators that play pleiotropic roles in cell differentiation, development, proliferation, and metabolic processes to govern liver physiology and pathology. Many nuclear receptors are ligand‐activated transcription factors that regulate the expression of their target genes by modulating transcriptional activities and epigenetic changes. Additionally, the protein complex associated with nuclear receptors consists of a multitude of coregulators, corepressors, and noncoding RNAs. Therefore, acquiring new information on nuclear receptors may provide invaluable insight into novel therapies and shed light on new interventions to reduce the burden and incidence of liver diseases. (Hepatology Communications 2018;2:765‐777)

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A Liver-Enriched Long Non-Coding RNA, lncLSTR, Regulates Systemic Lipid Metabolism in Mice

Cited by 258 publications

References 43 publications

Hepatic Gi signaling regulates whole-body glucose homeostasis

Hepatic Gi signaling regulates whole-body glucose homeostasis

Creation of Apolipoprotein C-II (ApoC-II) Mutant Mice and Correction of Their Hypertriglyceridemia with an ApoC-II Mimetic Peptide

Nuclear receptors and liver disease: Summary of the 2017 basic research symposium

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