Emerging roles of zinc finger proteins in regulating adipogenesis

Wei, Song; Zhang, Lifan; Zhou, Xiang; Du, Min; Jiang, Zhihua; Hausman, Gary; Bergen, Werner G.; Liu, Zan; Dodson, Michael V.

doi:10.1007/s00018-013-1395-0

Cited by 72 publications

(67 citation statements)

References 106 publications

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“…The difference between the Spearman correlation coefficient between random numbers and LEP values decreased asymptotically ( Figure 5f, right panel), and we further analyzed the genes displaying differences larger than 0.05 (Supplementary Tables 10 and 11). The gene most strongly positively correlated was ZNF395, which has been previously associated with adipogenesis [24,25], and pathways most enriched included the glycolysis pathway (genes ENO1 and ENO2) and pathways associated with pathogenic infection which are defined by cytoskeletal genes (Supplementary Table 11). The genes most negatively correlated included PAPPA (pappalysin), which regulates local bioavailability of IGF-1 and is differentially expressed in pre-adipocytes from different depots [26], and BSCL2, which is associated with lipid droplet formation and when mutated gives rise to congenital generalized lipodystrophy.…”

Section: Characteristics Of Progenitor Cells That Give Rise To Adipocmentioning

confidence: 99%

“Multiple human adipocyte subtypes and mechanisms of their development”

Desai

Yang

et al. 2019

Preprint

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Human adipose tissue depots perform numerous diverse physiological functions, and are differentially linked to metabolic disease risk, yet only two major human adipocyte subtypes have been described, white and "brown/brite/beige." The diversity and lineages of adipocyte classes have been studied in mice using genetic methods that cannot be applied in humans. Here we circumvent this problem by studying the fate of single mesenchymal progenitor cells obtained from human adipose tissue. We report that a minimum of four human adipocyte subtypes can be distinguished by transcriptomic analysis, specialized for functionally distinct processes such as adipokine secretion and thermogenesis. Evidence for the presence of these adipocytes subtypes in adult humans is evidenced by differential expression of key adipokines leptin and adiponectin in isolated mature adipocytes. The human adipocytes most similar to the mouse "brite/beige" adipocytes are enriched in mechanisms that promote iron accumulation and protect from oxidative stress, and are derived from progenitors that express high levels of cytokines such as IL1B, IL8, IL11 and the IL6 family cytokine LIF, and low levels of the transcriptional repressors ID1 and ID3. Our finding of this adipocyte repertoire and its developmental mechanisms provides a high-resolution framework to analyze human adipose tissue architecture and its role in systemic metabolism and metabolic disease.

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Section: Characteristics Of Progenitor Cells That Give Rise To Adipocmentioning

confidence: 99%

“Multiple human adipocyte subtypes and mechanisms of their development”

Desai

Yang

et al. 2019

Preprint

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show abstract

“…However, these aspects have yet to be fully elucidated. Transcriptional regulatory networks in commitment differentiation have also yet to be fully established although some transcription factors [5, 6] and signaling pathways have been confirmed [3]. As such, specific factors and molecular mechanisms involved in determination should be further investigated.…”

Section: Introductionmentioning

confidence: 99%

SIRT1 suppresses adipogenesis by activating Wnt/β-catenin signaling in vivo and in vitro

et al. 2016

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Sirtuin 1 (SIRT1) regulates adipocyte and osteoblast differentiation. However, the underlying mechanism should be investigated. This study revealed that SIRT1 acts as a crucial repressor of adipogenesis. RNA-interference-mediated SIRT1 knockdown or genetic ablation enhances adipogenic potential, whereas SIRT1 overexpression inhibits adipogenesis in mesenchymal stem cells (MSCs). SIRT1 also deacetylates the histones of sFRP1, sFRP2, and Dact1 promoters; inhibits the mRNA expression of sFRP1, sFRP2, and Dact1; activates Wnt signaling pathways; and suppresses adipogenesis. SIRT1 deacetylates β-catenin to promote its accumulation in the nucleus and thus induces the transcription of genes that block MSC adipogenesis. In mice, the partial absence of SIRT1 promotes the formation of white adipose tissues without affecting the development of the body of mice. Our study described the regulatory role of SIRT1 in Wnt signaling and proposed a regulatory mechanism of adipogenesis.

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“…Among the genes with differentially methylated CpG sites, ZNF154 encodes a member of the zinc finger protein family, which are transcriptional regulators of adipogenesis [17]. POLR3E encodes DNA-directed RNA polymerase III subunit RPC5, and it is known that the loss of MAF , which is a repressor of RNA polymerase III, affects resistance to obesity [18].…”

Section: Resultsmentioning

confidence: 99%

DNA Methylation Profiles of Blood Cells Are Distinct between Early-Onset Obese and Control Individuals

et al. 2017

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Obesity is a highly prevalent, chronic disorder that has been increasing in incidence in young patients. Both epigenetic and genetic aberrations may play a role in the pathogenesis of obesity. Therefore, in-depth epigenomic and genomic analyses will advance our understanding of the detailed molecular mechanisms underlying obesity and aid in the selection of potential biomarkers for obesity in youth. Here, we performed microarray-based DNA methylation and gene expression profiling of peripheral white blood cells obtained from six young, obese individuals and six healthy controls. We observed that the hierarchical clustering of DNA methylation, but not gene expression, clearly segregates the obese individuals from the controls, suggesting that the metabolic disturbance that occurs as a result of obesity at a young age may affect the DNA methylation of peripheral blood cells without accompanying transcriptional changes. To examine the genome-wide differences in the DNA methylation profiles of young obese and control individuals, we identified differentially methylated CpG sites and investigated their genomic and epigenomic contexts. The aberrant DNA methylation patterns in obese individuals can be summarized as relative gains and losses of DNA methylation in gene promoters and gene bodies, respectively. We also observed that the CpG islands of obese individuals are more susceptible to DNA methylation compared to controls. Our pilot study suggests that the genome-wide aberrant DNA methylation patterns of obese individuals may advance not only our understanding of the epigenomic pathogenesis but also early screening of obesity in youth.

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Emerging roles of zinc finger proteins in regulating adipogenesis

Cited by 72 publications

References 106 publications

“Multiple human adipocyte subtypes and mechanisms of their development”

“Multiple human adipocyte subtypes and mechanisms of their development”

SIRT1 suppresses adipogenesis by activating Wnt/β-catenin signaling in vivo and in vitro

DNA Methylation Profiles of Blood Cells Are Distinct between Early-Onset Obese and Control Individuals

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