Adipocyte differentiation from the inside out

Rosen, Evan D.; MacDougald, Ormond A.

doi:10.1038/nrm2066

Cited by 2,212 publications

(2,185 citation statements)

References 149 publications

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“…Once the differentiation switches were activated and opened, MSCs then initiated adipogenesis by activating expression of adipogenic genes such as FABP4, leptin, and adiponection 19. Many studies confirmed that most growth factors or stimuli that upregulated adipogenesis ultimately exerted their effects through regulation of PPARγ and C/EBPα expression 20. In the present study, we found that Si ions strongly enhanced expression of PPARγ and C/EBPα in adipogenic‐induced cells.…”

Section: Discussionsupporting

confidence: 60%

Silicon‐Enhanced Adipogenesis and Angiogenesis for Vascularized Adipose Tissue Engineering

et al. 2018

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The enhancement of adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and sufficient vascularization remain great challenges for the successful reconstruction of engineered adipose tissue. Here, the bioactive effects of silicon (Si) ions on adipogenic differentiation of human BMSCs (HBMSCs) and the stimulation of vascularization during adipose tissue regeneration are reported. The results show that Si ions can enhance adipogenic differentiation of HBMSCs through the stimulation of the expression of adipogenic differentiation switches such as peroxisome proliferator‐activated receptor γ and CCAAT/enhancer‐binding protein α. Furthermore, Si ions can enhance both angiogenesis and adipogenesis, and inhibit dedifferentiation of cocultured adipocytes by regulating the interactions between HBMSC‐derived adipocytes and human umbilical vein endothelial cells, in which the promotion of the expression of insulin‐like growth factor 1 and vascular endothelial growth factor plays vital roles. The in vivo studies further demonstrate that the designed composite hydrogel with the ability to release bioactive Si ions clearly stimulates neovascularization and adipose tissue regeneration. The study suggests that Si ions released from biomaterials are important chemical cues for adipogenic differentiation and biomaterials with the ability to release Si ions can be designed for adipose tissue engineering.

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Section: Discussionsupporting

confidence: 60%

Silicon‐Enhanced Adipogenesis and Angiogenesis for Vascularized Adipose Tissue Engineering

et al. 2018

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“…In the 3T3-L1 model, C/EBPb and C/EBPd are rapidly activated upon induction of differentiation. They in turn induce C/EBPa and PPARg2, which together activate the majority of genes expressed in differentiating adipocytes (Rosen and MacDougald, 2006). To address the molecular mechanisms underlying hSNF5/INI1-mediated adipogenic differentiation, we investigated the expression To further study the cooperation between hSNF5/ INI1 and C/EBPb, we carried out transcription activation reporter assays with the PPARg2 promoter, which has been described previously to contain C/EBP binding sites and to be activated by C/EBP proteins (Saladin et al, 1999).…”

Section: Requirement For Snf5/ini1 In Adipogenic Differentiation Modelsmentioning

confidence: 99%

The requirement for SNF5/INI1 in adipocyte differentiation highlights new features of malignant rhabdoid tumors

et al. 2007

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ATP-dependent SWI/SNF chromatin remodeling complexes regulate cell-cycle and play critical roles in a variety of differentiation pathways. The core subunit SNF5/INI1 is a tumor suppressor that is inactivated in a highly aggressive childhood cancer of unknown cellular origin, termed malignant rhabdoid tumor (MRT). The highly undifferentiated phenotype of this tumor suggests that the loss-of-function of hSNF5/INI1 impairs specific differentiation programs of the MRT parental cell. Based on the hypothesis that these programs might be reinitialized upon hSNF5/INI1 re-expression in MRTs, we show that some MRT cell lines can differentiate toward the adipogenic lineage. We further show that the knock down of the SNF5/INI1 subunit abrogates adipocyte differentiation of murine 3T3-L1 preadipocytes and of human mesenchymal stem cells. Finally, we provide evidence that hSNF5/INI1 cooperates with C/EBPb and PPARc2 transcriptional regulators to activate the expression of adipocyte-specific genes. These data indicate that not only the ATPase subunit of the SWI/SNF complex, but also SNF5/INI1 is required for adipocyte differentiation. They further show that MRT cell lines harbor an adipogenic differentiation potential and that the tumor suppressor role of the SNF5/INI1 subunit may rely on its ability to regulate the balance between cell proliferation and differentiation.

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“…WAT primarily contributes to energy storage and the regulation of energy balance at large. [1][2][3] BAT's principal function is to generate heat by fat burning. 4 Disruption of normal metabolic homeostasis in obesity leads to the development of several pathological conditions such as insulin resistance, type 2 diabetes and increased risk of development of a variety of cancers.…”

mentioning

confidence: 99%

“…Being both necessary and sufficient for white and brown adipocyte formation, PPARg is considered to be the master regulator of adipogenesis. 1,3 The brown adipocyte shares a common progenitor cell with the skeletal muscle lineage. The transcription factor Positive-Regulatory-Domain-Containing-16 (PRDM16) has been identified as the key molecular switch committing skeletal muscle progenitors into the development of brown adipocytes.…”

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confidence: 99%

p53 is required for brown adipogenic differentiation and has a protective role against diet-induced obesity

et al. 2013

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Proper regulation of white and brown adipogenic differentiation is important for maintaining an organism's metabolic profile in a homeostatic state. The recent observations showing that the p53 tumor suppressor plays a role in metabolism raise the question of whether it is involved in the regulation of white and brown adipocyte differentiation. By using several in vitro models, representing various stages of white adipocyte differentiation, we found that p53 exerts a suppressive effect on white adipocyte differentiation in both mouse and human cells. Moreover, our in vivo analysis indicated that p53 is implicated in protection against diet-induced obesity. In striking contrast, our data shows that p53 exerts a positive regulatory effect on brown adipocyte differentiation. Abrogation of p53 function in skeletal muscle committed cells reduced their capacity to differentiate into brown adipocytes and histological analysis of brown adipose tissue revealed an impaired morphology in both embryonic and adult p53-null mice. Thus, depending on the specific adipogenic differentiation program, p53 may exert a positive or a negative effect. This cell type dependent regulation reflects an additional modality of p53 in maintaining a homeostatic state, not only in the cell, but also in the organism at large.

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Adipocyte differentiation from the inside out

Cited by 2,212 publications

References 149 publications

Silicon‐Enhanced Adipogenesis and Angiogenesis for Vascularized Adipose Tissue Engineering

Silicon‐Enhanced Adipogenesis and Angiogenesis for Vascularized Adipose Tissue Engineering

The requirement for SNF5/INI1 in adipocyte differentiation highlights new features of malignant rhabdoid tumors

p53 is required for brown adipogenic differentiation and has a protective role against diet-induced obesity

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