Albumin expression is required for adipocyte differentiation of 3T3-L1 cells

Yoo, Wonbaek; Lee, Jaeseob; Park, Sangeun; Kim, Young Sik; Lim, Chae Woo; Yoon, Eul Sik; Hur, Gang Min; Oh, Junseo

doi:10.1016/j.bbrc.2010.05.067

Cited by 13 publications

(11 citation statements)

References 26 publications

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“…This finding strengthens our notion that albumin is required for the acquisition and maintenance of fat-storing phenotype and suggests that albumin can be used as a reliable marker for the activation status of stellate cells. Critical role of albumin in cytoplasmic lipid droplet formation was also demonstrated during 3T3-L1 adipocyte differentiation (Yoo et al, 2010), and its expression was recently reported in human adipocytes (Sirico et al, 2012). It remains unclear how albumin promotes lipid droplet formation in 3T3-L1 and HSCs.…”

Section: Discussionmentioning

confidence: 96%

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

Park

Choi

Lee

et al. 2012

Molecules and Cells

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Liver fibrosis is characterized by accumulation of extracellular matrix, and activated hepatic stellate cells (HSCs) are the primary source of the fibrotic neomatrix and considered as therapeutic target cells. We previously showed that albumin in pancreatic stellate cells (PSCs), the key cell type for pancreatic fibrogenesis, is directly involved in the formation of vitamin A-containing lipid droplets, inhibiting PSC activation. In this study, we evaluated the anti-fibrotic activity of both albumin and retinol binding protein-albumin domain III fusion protein (R-III), designed for stellate cell-targeted delivery of albumin III, in rat primary HSCs and investigated the underlying mechanism. Forced expression of albumin or R-III in HSCs after passage 2 (activated HSCs) induced lipid droplet formation and deactivated HSCs, whereas point mutations in high-affinity fatty acid binding sites of albumin domain III abolished their activities. Exogenous R-III, but not albumin, was successfully internalized into and deactivated HSC-P2. When HSCs at day 3 after plating (pre-activated HSCs) were cultured in the presence of purified R-III, spontaneous activation of HSCs was inhibited even after passage 2, suggestive of a potential for preventive effect. Furthermore, treatment of HSCs-P2 with R-III led to a significant reduction in both cytoplasmic levels of all-trans retinoic acid and the subsequent retinoic acid signaling. Therefore, our data suggest that albumin deactivates HSCs with reduced retinoic acid levels and that R-III may have therapeutic and preventive potentials on liver fibrosis.

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Section: Discussionmentioning

confidence: 96%

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

Park

Choi

Lee

et al. 2012

Molecules and Cells

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“…In fact, Yoo and Lee investigated the role of albumin in adipocyte differentiation, by using pre-adipocytes cell lines such as 3T3-L1 [26]. This is a developmental process by which undifferentiated precursor cells differentiate into mature adipocytes with coordinated changes in cell morphology and gene expression.…”

Section: Discussionmentioning

confidence: 99%

“…This is a developmental process by which undifferentiated precursor cells differentiate into mature adipocytes with coordinated changes in cell morphology and gene expression. They found that albumin gene expression was significantly increased at later stages of adipocyte differentiation process and its suppression significantly inhibited lipid droplet formation [26]. The author suggests that albumin could be necessary to stabilize lipid accumulation in mature adipocyte, probably through a direct interaction with fatty acids.…”

Section: Discussionmentioning

confidence: 99%

Human Mature Adipocytes Express Albumin and This Expression Is Not Regulated by Inflammation

Sirico

Guida²,

Procino

et al. 2012

Mediators of Inflammation

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Aims. Our group investigated albumin gene expression in human adipocytes, its regulation by inflammation and the possible contribution of adipose tissue to albumin circulating levels. Methods. Both inflamed and healthy subjects provided adipose tissue samples. RT-PCR, Real-Time PCR, and Western Blot analysis on homogenates of adipocytes and pre-adipocytes were performed. In sixty-three healthy subjects and fifty-four micro-inflamed end stage renal disease (ESRD) patients circulating levels of albumin were measured by nephelometry; all subjects were also evaluated for body composition, calculated from bioelectrical measurements and an thropometric data. Results. A clear gene expression of albumin was showed in pre-adipocytes and, for the first time, in mature adipocytes. Albumin gene expression resulted significantly higher in pre-adipocytes than in adipocytes. No significant difference in albumin gene expression was showed between healthy controls and inflamed patients. A significant negative correlation was observed between albumin levels and fat mass in both healthy subjects and inflamed ESRD patients. Conclusions. In the present study we found first time evidence that human adipocytes express albumin. Our results also showed that systemic inflammation does not modulate albumin gene expression. The negative correlation between albumin and fat mass seems to exclude a significant contributing role of adipocyte in plasma albumin.

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“…Some of them involved in maturation of adipocytes, such as miR-1431, 2, miR-369-5p3, miR-27a/b4, 5. However, it is far from understanding their functions and mechanisms completely.…”

Section: Introductionmentioning

confidence: 99%

Up-regulated miR-145 Expression Inhibits Porcine Preadipocytes Differentiation by Targeting IRS1

Guo¹,

Chen²,

Zhang³

et al. 2012

Int. J. Biol. Sci.

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Generally, most miRNAs that were up-regulated during differentiation promoted adipogenesis, but our research indicated that up-regulation of miR-145 in porcine preadipocytes did not promote but inhibit adipogenesis. In this study, miR-145 was significantly up-regulated during porcine dedifferentiated fat (DFAT) cells differentiation. In miR-145 overexpressed DFAT cells, adipogenesis was inhibited and triglycerides accumulation was decreased after hormone stimulation (P<0.05). Furthermore, up-regulation of miR-145 expression repressed induction of mRNA levels of adipogenic markers, such as CCAAT/enhancer-binding protein α (C/EBPα), and peroxisome proliferator-activated receptor γ2 (PPARγ2). These effects caused by miR-145 overexpression were mediated by Insulin receptor substrate 1 (IRS1) as a mechanism. These data suggested that induced miR-145 expression during differentiation could inhibit adipogenesis by targeting IRS1, and miR-145 may be novel agent for adipose tissue engineering.

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Albumin expression is required for adipocyte differentiation of 3T3-L1 cells

Cited by 13 publications

References 26 publications

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

Retinol Binding Protein-Albumin Domain III Fusion Protein Deactivates Hepatic Stellate Cells

Human Mature Adipocytes Express Albumin and This Expression Is Not Regulated by Inflammation

Up-regulated miR-145 Expression Inhibits Porcine Preadipocytes Differentiation by Targeting IRS1

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