Mouse Embryonic Fibroblast Adipogenic Potential: A Comprehensive Transcriptome Analysis

Al-Sayegh, Mohamed; Ali, Hamad; Jamal, Mohammad H.; ElGindi, Mei; Chanyong, Tina; Al-Awadi, Khulood; Abu‐Farha, Mohamed

doi:10.1080/21623945.2020.1859789

Cited by 9 publications

(4 citation statements)

References 116 publications

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“…While a variety of myosin types are implicated in adipocyte metabolism, little is known about the role of MYH10 in adipocytes and adipogenesis. Previous studies have reported that MYH10 is expressed in adipocytes 29,[35][36][37][38] , and we have previously demonstrated the association of reorganized actin filaments and other candidate proteins, including MYH10, in adipocyte differentiation 6 . However, the mechanism of action and function of MYH10 in adipocytes has never been studied.…”

Section: Introductionmentioning

confidence: 59%

MYH10 governs adipocyte function and adipogenesis through its interaction with GLUT4

Kislev

Moldovan

Barak

et al. 2021

Preprint

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Adipocyte differentiation is dependent on cytoskeletal remodeling processes that determine and maintain cellular shape and function. In turn, cytoskeletal proteins contribute to the filament-based network responsible for controlling adipocyte's shape and promoting the intracellular trafficking of key cellular components. Currently, our understanding of these mechanisms remains incomplete. In this study, we identified the non-muscle myosin 10 (MYH10) as an important regulator of adipogenesis and adipocyte function through its interaction with the insulin dependent, Glucose transporter 4 (GLUT4). MYH10 depletion in preadipocytes resulted in impaired adipogenesis, with knockdown cells exhibiting disrupted morphology and reduced molecular adipogenic signals. MYH10 was shown to be in complex with GLUT4 in adipocytes, an interaction regulated by insulin induction. The missing adipogenic capacity of MYH10-KD cells was restored when they uptook GLUT4 vesicles up from neighbor wild-type cells in a co-culture system. Our results provide the first demonstration that MYH10 interacts with GLUT4 in cells and adipose tissue through the insulin pathway. The signaling cascade is regulated by the protein kinase C ζ (PKCζ), which interacts with MYH10 to modify the localization and interaction of both GLUT4 and MYH10 in adipocytes as PKCζ inhibition resulted in reduced GLUT4 and MYH10 translocation and interactions. Overall, our study establishes MYH10 as an essential regulator of GLUT4 translocation, affecting both adipogenesis and adipocyte function, highlighting its importance in future cytoskeleton-based studies in adipocytes.

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Section: Introductionmentioning

confidence: 59%

MYH10 governs adipocyte function and adipogenesis through its interaction with GLUT4

Kislev

Moldovan

Barak

et al. 2021

Preprint

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“…As an additional test that HMGN proteins can modulate adipocyte browning, we differentiated mouse embryonic fibroblasts (MEFs) from WT and DKO mice into adipocytes using a cocktail known to facilitate differentiation into brown-like adipocytes 14 , 35 , 36 (Fig. S 8a ).…”

Section: Resultsmentioning

confidence: 99%

Epigenetic regulation of white adipose tissue plasticity and energy metabolism by nucleosome binding HMGN proteins

et al. 2022

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White adipose tissue browning is a key metabolic process controlled by epigenetic factors that facilitate changes in gene expression leading to altered cell identity. We find that male mice lacking the nucleosome binding proteins HMGN1 and HMGN2 (DKO mice), show decreased body weight and inguinal WAT mass, but elevated food intake, WAT browning and energy expenditure. DKO white preadipocytes show reduced chromatin accessibility and lower FRA2 and JUN binding at Pparγ and Pparα promoters. White preadipocytes and mouse embryonic fibroblasts from DKO mice show enhanced rate of differentiation into brown-like adipocytes. Differentiating DKO adipocytes show reduced H3K27ac levels at white adipocyte-specific enhancers but elevated H3K27ac levels at brown adipocyte-specific enhancers, suggesting a faster rate of change in cell identity, from white to brown-like adipocytes. Thus, HMGN proteins function as epigenetic factors that stabilize white adipocyte cell identity, thereby modulating the rate of white adipose tissue browning and affecting energy metabolism in mice.

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“…By using NCBI SRA toolkit, the raw metadata was downloaded from the FASTQ files of Gene Expression Omnibus (GEO) datasets: (i) GSE138242: 20-week old visceral adipose tissue (vAT) from chow diet (CD)-fed mice (n = 3) and high fat diet (HFD)-fed mice (n = 3), 43 (ii) GSE55008: omental adipose tissue (oAT) from lean control (n = 12) and obese patients (n = 12), 44 and (iii) GSE152750: undifferentiated mouse embryo fibroblast (MEF) (n = 3) and differentiated MEF (n = 3) for 5 d in AIM. 45 The transcriptomic RNA-seq was performed using TopHat2 aligner (https://ccb.jhu.edu/softw are/topha t/index.shtml) and Cufflinks assembler (http://cole-trapn ell-lab.github.io/ cuffl inks) with mouse reference gene mm10 and human reference gene hg19. The transcript expression was calculated as Fragments Per Kilobase of transcript per Million fragments mapped (FPKM).…”

Section: Big Data Analysis and Gene Expression Profilesmentioning

confidence: 99%

Caveolin‐2 in association with nuclear lamina controls adipocyte hypertrophy

2023

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Here, we identify that Caveolin‐2 (Cav‐2), an integral membrane protein, controls adipocyte hypertrophy in association with nuclear lamina. In the hypertrophy stage of adipogenesis, pY19‐Cav‐2 association with lamin A/C facilitated the disengagement of CCAAT/enhancer‐binding protein α (C/EBPα) and peroxisome proliferator‐activated receptor γ (PPARγ) from lamin A/C and repressed Cav‐2 promoter at the nuclear periphery for epigenetic activation of Cav‐2, and thereby promoted C/EBPα and PPARγ‐induced adipocyte hypertrophy. Stable expression of Cav‐2 was required and retained by phosphorylation, deubiquitination, and association with lamin A/C for the adipocyte hypertrophy. However, obese adipocytes exhibited augmented Cav‐2 stability resulting from the up‐regulation of lamin A/C over lamin B1, protein tyrosine phosphatase 1B (PTP1B), and nuclear deubiquitinating enzyme (DUB), Uchl5. Our findings show a novel epigenetic regulatory mechanism of adipocyte hypertrophy by Cav‐2 at the nuclear periphery.

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Mouse Embryonic Fibroblast Adipogenic Potential: A Comprehensive Transcriptome Analysis

Cited by 9 publications

References 116 publications

MYH10 governs adipocyte function and adipogenesis through its interaction with GLUT4

MYH10 governs adipocyte function and adipogenesis through its interaction with GLUT4

Epigenetic regulation of white adipose tissue plasticity and energy metabolism by nucleosome binding HMGN proteins

Caveolin‐2 in association with nuclear lamina controls adipocyte hypertrophy

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