TET2 is recruited by CREB to promote Cebpb, Cebpa, and Pparg transcription by facilitating hydroxymethylation during adipocyte differentiation

Liu, Yunjia; He, Ting; Li, Zhuofang; Sun, Zhen; Wang, Shuai; Shen, Huanming; Hou, Lingfeng; Li, Shengnan; Wei, Yixin; Zhuo, Bingzhao; Li, Shanni; Zhou, Can; Guo, Huiling; Zhang, Rui; Li, Boan

doi:10.1016/j.isci.2023.108312

Cited by 4 publications

(1 citation statement)

References 52 publications

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“…The results of the Oil Red O staining and triglyceride content assay showed a significant increase in lipid droplet accumulation in chicken abdominal adipocytes. The expression levels of PPARG and CEBPA were significantly altered by SLC22A16 , and there is ample evidence to suggest that PPARG and CEBPA are the main transcription factors involved in adipocyte differentiation [ 50 , 51 , 52 ]. lncRNAs are important regulatory molecules and actively participate in various biological processes [ 53 , 54 , 55 , 56 ].…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA 6302 Regulates Chicken Preadipocyte Differentiation by Targeting SLC22A16

Ma,

He,

Liu

et al. 2024

Genes

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The excessive deposition of abdominal adipocytes in chickens is detrimental to poultry production. However, the regulatory factors that affect abdominal adipogenesis in chickens are still poorly understood. SLC22A16 is differentially expressed in abdominal preadipocytes and 10-day differentiated adipocytes in chickens, but its role in regulating chicken adipogenesis has not been reported. In this study, the function of SLC22A16 in chicken abdominal preadipocytes was investigated. SLC22A16 is significantly upregulated during abdominal adipocyte differentiation. The overexpression of SLC2A16 upregulated the expression of adipogenic marker genes and proliferation-related genes, and promoted the proliferation of adipocytes and the accumulation of triglycerides. The knockdown of SLC22A16 downregulated the expression of adipogenic marker genes and proliferation-related genes, inhibited the proliferation of adipocytes, and impaired the accumulation of triglycerides in adipocytes. In addition, LNC6302 was differentially expressed in abdominal preadipocytes and mature adipocytes, and was significantly positively correlated with the expression of SLC22A16. Interference with LNC6302 inhibits the expression of adipogenic marker genes and proliferation-related genes. The data supported the notion that LNC6302 promotes the differentiation of chicken abdominal adipocytes by cis-regulating the expression of SLC22A16. This study identified the role of SLC22A16 in the differentiation and proliferation of chicken adipocytes, providing a potential target for improving abdominal adipogenesis in chickens.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA 6302 Regulates Chicken Preadipocyte Differentiation by Targeting SLC22A16

Ma,

He,

Liu

et al. 2024

Genes

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Beyond genetics: Exploring the role of epigenetic alterations in breast cancer

Prabhu,

Sadida,

Kuttikrishnan

et al. 2024

Pathology - Research and Practice

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Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

Lobato,

Salomón-Soto,

Espinosa-Méndez

et al. 2024

Biomolecules

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Obesity, influenced by environmental pollutants, can lead to complex metabolic disruptions. This systematic review and meta-analysis examined the molecular mechanisms underlying metabolically abnormal obesity caused by exposure to a high-fat diet (HFD) and fine particulate matter (PM2.5). Following the PRISMA guidelines, articles from 2019 to 2024 were gathered from Scopus, Web of Science, and PubMed, and a random-effects meta-analysis was performed, along with subgroup analyses and pathway enrichment analyses. This study was registered in the Open Science Framework. Thirty-three articles, mainly case–control studies and murine models, were reviewed, and they revealed that combined exposure to HFD and PM2.5 resulted in the greatest weight gain (82.835 g, p = 0.048), alongside increases in high-density lipoproteins, insulin, and the superoxide dismutase. HFD enriched pathways linked to adipocytokine signaling in brown adipose tissue, while PM2.5 impacted genes associated with fat formation. Both exposures downregulated protein metabolism pathways in white adipose tissue and activated stress-response pathways in cardiac tissue. Peroxisome proliferator-activated receptor and AMP-activated protein kinase signaling pathways in the liver were enriched, influencing non-alcoholic fatty liver disease. These findings highlight that combined exposure to HFD and PM2.5 amplifies body weight gain, oxidative stress, and metabolic dysfunction, suggesting a synergistic interaction with significant implications for metabolic health.

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TET2 is recruited by CREB to promote Cebpb, Cebpa, and Pparg transcription by facilitating hydroxymethylation during adipocyte differentiation

Cited by 4 publications

References 52 publications

Long Noncoding RNA 6302 Regulates Chicken Preadipocyte Differentiation by Targeting SLC22A16

Long Noncoding RNA 6302 Regulates Chicken Preadipocyte Differentiation by Targeting SLC22A16

Beyond genetics: Exploring the role of epigenetic alterations in breast cancer

Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis

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