Whole Transcriptome Analysis Reveals a Potential Regulatory Mechanism of LncRNA-FNIP2/miR-24-3p/FNIP2 Axis in Chicken Adipogenesis

Guo, Lingling; Chao, Xiaohuan; Huang, Weiling; Li, Zhenhui; Luan, Kang; Ye, Mao; Zhang, Siyu; Liu, Yijie; Li, Hongmei; Luo, Wen; Nie, Qinghua; Zhang, Xiquan; Luo, Qianyi

doi:10.3389/fcell.2021.653798

Cited by 18 publications

(10 citation statements)

References 60 publications

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“…These studies provided new insights into the molecular mechanisms to explore fat metabolism in pigs. Also, the study found there was a lncRNA-FNIP2/miR-24-3p/FNIP2 axis, which can regulate lipid metabolism in Sanghuang chicken liver ( Guo et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

MiRNA-Seq reveals key MicroRNAs involved in fat metabolism of sheep liver

Fei

Jin²,

Yuan³

et al. 2023

Front. Genet.

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There is a genetic difference between Hu sheep (short/fat-tailed sheep) and Tibetan sheep (short/thin-tailed sheep) in tail type, because of fat metabolism. Previous studies have mainly focused directly on sheep tail fat, which is not the main organ of fat metabolism. The function of miRNAs in sheep liver fat metabolism has not been thoroughly elucidated. In this study, miRNA-Seq was used to identify miRNAs in the liver tissue of three Hu sheep (short/fat-tailed sheep) and three Tibetan sheep (short/thin-tailed sheep) to characterize the differences in fat metabolism of sheep. In our study, Hu sheep was in a control group, we identified 11 differentially expressed miRNAs (DE miRNAs), including six up-regulated miRNAs and five down-regulated miRNAs. Miranda and RNAhybrid were used to predict the target genes of DE miRNAs, obtaining 3,404 target genes. A total of 115 and 67 GO terms as well as 54 and 5 KEGG pathways were significantly (padj < 0.05) enriched for predicted 3,109 target genes of up-regulated and 295 target genes of down-regulated miRNAs, respectively. oar-miR-432 was one of the most up-regulated miRNAs between Hu sheep and Tibetan sheep. And SIRT1 is one of the potential target genes of oar-miR-432. Furthermore, functional validation using the dual-luciferase reporter assay indicated that the up-regulated miRNA; oar-miR-432 potentially targeted sirtuin 1 (SIRT1) expression. Then, the oar-miR-432 mimic transfected into preadipocytes resulted in inhibited expression of SIRT1. This is the first time reported that the expression of SIRT1 gene was regulated by oar-miR-432 in fat metabolism of sheep liver. These results could provide a meaningful theoretical basis for studying the fat metabolism of sheep.

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Section: Discussionmentioning

confidence: 99%

MiRNA-Seq reveals key MicroRNAs involved in fat metabolism of sheep liver

Fei

Jin²,

Yuan³

et al. 2023

Front. Genet.

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“…The immortalized chicken preadipocyte cell line (ICP1) was obtained from the Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture and Rural Affairs, Northeast Agricultural University (Harbin, China). The ICP1 cell line was established by infecting chicken stromal-vascular cells with a recombinant retrovirus expressing chicken telomerase RNA [11] ; these cells share common morphology and differentiation features with primary preadipocytes and are widely used in chicken adipogenesis studies [ 14 – 16 ] . ICP1 and DF-1 cell lines (ATCC, Manassas, USA) were cultured in DMEM F-12 (Gibco, Carlsbad, USA) and DMEM high glucose (Gibco) respectively, supplemented with 10% fetal bovine serum (Gibco) and maintained at 37°C in a 5% CO 2 cell incubator [ 11 , 17 ] .…”

Section: Methodsmentioning

confidence: 99%

PU.1 interacts with KLF7 to suppress differentiation and promote proliferation in chicken preadipocytes

Tan¹,

Xu²,

Li³

et al. 2023

ABBS

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Krüppel-like factor 7 (KLF7) is a negative regulator of preadipocyte differentiation. Our previous KLF7 ChIP-seq analysis showed that the binding motif of PU.1 was found among the KLF7 binding peaks, indicating that an interaction between KLF7 and PU.1 at preadipocyte gene promoters and other regulatory elements might be common. Here, Co-IP and FRET assays are used to confirm that PU.1 can directly bind to KLF7 and enhance the transcription activity of cyclin-dependent kinase inhibitor 3 ( CDKN3 ), which is a downstream target gene of KLF7. We show that the PU.1 expression level is decreased during preadipocyte differentiation. Furthermore, PU.1 overexpression and knockdown experiments reveal that PU.1 negatively regulates chicken preadipocyte differentiation, as evidenced by appropriate changes in lipid droplet accumulation and altered expressions of PPARγ, FAS, and PLIN. In addition, PU.1 overexpression promotes preadipocyte proliferation, while knockdown of PU . 1 inhibits preadipocyte proliferation. We further demonstrate that PU.1 inhibits differentiation and promotes proliferation in preadipocytes, in part by directly interacting with KLF7.

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“…The immortalized chicken preadipocyte ICP1 [24] and chicken fibroblast DF-1 [25] cell lines were kindly provided by the Key Laboratory of Chicken Genetics and Breeding, Ministry of Agriculture and Rural Affairs, Northeast Agricultural University (Harbin, China). ICP1 cells have been widely used to study chicken adipogenesis [26, 27], as they present the same morphological and differentiation characteristics as primary preadipocytes [24, 26, 27]. DF-1, an immortalized chicken fibroblast cell line, can be easily transiently transfected with exogenous DNA.…”

Section: Methodsmentioning

confidence: 99%

KLF7 Promotes Preadipocyte Proliferation via Activation of the Akt Signaling Pathway by Cis-regulating CDKN3

Jia

Jin

et al. 2022

Preprint

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Kruppel-like transcription factor 7 (KLF7) promotes preadipocyte proliferation; however, its target gene in this process has not yet been identified. Using KLF7 ChIP-seq analysis, we previously showed that a KLF7-binding peak is present upstream of the cyclin-dependent kinase inhibitor 3 gene (CDKN3) in chicken preadipocytes. In the current study, we identified CDKN3 as a target gene of KLF7 that mediates the effects of KLF7 on preadipocyte proliferation. Furthermore, 5 ′ -truncating mutation analysis showed that the minimal promoter was located between CDKN3 nt -160 and nt -7 (relative to the translation initiation codon ATG). KLF7 overexpression increased CDKN3 promoter activity in the DF-1 and immortalized chicken preadipocyte (ICP1) cell lines. Deletion of the putative binding site of KLF7 abolished the promotive effect of KLF7 overexpression on CDKN3 promoter activity. Moreover, CDKN3 -knockdown and -overexpression assays revealed that CDKN3 enhanced ICP1 cell proliferation. Flow cytometry analysis showed that CDKN3 accelerated the G1/S transition. Further, we found that KLF7 promoted ICP1 cell proliferation via Akt phosphorylation by regulating CDKN3. Taken together, these results suggest that KLF7 promotes preadipocyte proliferation via activating the Akt signaling pathway by cis – regulating CDKN3, thus driving the G1/S transition.

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Whole Transcriptome Analysis Reveals a Potential Regulatory Mechanism of LncRNA-FNIP2/miR-24-3p/FNIP2 Axis in Chicken Adipogenesis

Cited by 18 publications

References 60 publications

MiRNA-Seq reveals key MicroRNAs involved in fat metabolism of sheep liver

MiRNA-Seq reveals key MicroRNAs involved in fat metabolism of sheep liver

PU.1 interacts with KLF7 to suppress differentiation and promote proliferation in chicken preadipocytes

KLF7 Promotes Preadipocyte Proliferation via Activation of the Akt Signaling Pathway by Cis-regulating CDKN3

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