Up-regulation of adipogenin, an adipocyte plasma transmembrane protein, during adipogenesis

Hong, Yeon Hee; Hishikawa, Daisuke; Miyahara, Hisae; Tsuzuki, Hiroaki; Nishimura, Yukihiko; Gotoh, Chizu; Choi, Ki Choon; Hokari, Yu; Takagi, Yuji; Lee, Hong Gu; Cho, Kwang Keun; Roh, Sang Gun; Sasaki, Shinichi

doi:10.1007/s11010-005-3673-0

Cited by 30 publications

(33 citation statements)

References 23 publications

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“…Stem cell isolation procedure was performed as described previously [Gimble and Guilak, 2003a;Hong et al, 2005;Niemela et al, 2007]. Briefly, human adipose tissue specimens were cut into small pieces, enzymatically digested with 0.05% collagenase I (Invitrogen, Paisley, UK) in Dulbecco's Modified Eagle's Medium Nutrient Mixture F-12 (Gibco, Invitrogen, Carlsbad, Calif., USA) for 60 min at 37 ° C in a gyratory water bath.…”

Section: Isolation and Culture Of Hascsmentioning

confidence: 99%

Adipose Stromal Cell Tubule Network Model Provides a Versatile Tool for Vascular Research and Tissue Engineering

Sarkanen

Vuorenpää²,

Huttala³

et al. 2012

Cells Tissues Organs

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The current limitation in designing three-dimensional tissue models is the lack of adequate vascularization with mature and stable vessels. Adipose tissue is known to secrete several angiogenic factors, and human adipose stromal cells (hASC) are known to promote vessel growth, maturation and stabilization. In this study, hASC were induced to angiogenesis with growth factor-enriched medium either in monoculture or in coculture with human umbilical vein endothelial cells (HUVEC) and analyzed for vascular, pericytic and smooth muscle cell markers. hASC and HUVEC cocultures showed an accelerated proliferation rate and the cells self-assembled, independent of the cell passage number, into multilayered three-dimensional tubular networks. The networks of hASC and HUVEC expressed endothelial markers, a complete basement membrane and vessel-supporting cells with contractile properties. A hASC and green fluorescence protein-HUVEC-infection model revealed that cocultures consisted of a mosaic of von Willebrand factor-positive cells derived from both cell populations – hASC and HUVEC. hASC monoculture had passage- and donor-dependent ability to form tubular networks, with half of the cultures presenting tubule structures and basement membrane formation. Pericytic and smooth muscle cell markers were expressed in hASC monoculture even when tubules were absent. By combining the potential properties of hASC and features from the present angiogenesis assays, we generated a natural-like, xeno-free, prevascular-like network in vitro model with excellent reproducibility and minimal limitations in technical performance. This tubular network model is an excellent tool for studying cell interactions during vascular development, for chemical and drug testing and for developing natural-like, multilayered, vascularized, scaffold-free tissue models.

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Section: Isolation and Culture Of Hascsmentioning

confidence: 99%

Adipose Stromal Cell Tubule Network Model Provides a Versatile Tool for Vascular Research and Tissue Engineering

Sarkanen

Vuorenpää²,

Huttala³

et al. 2012

Cells Tissues Organs

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“…This was because a report by Hong and coworkers (wherein Smaf1 was named Adipogenin) indicated that knockdown of Smaf1 in preadipocytes, followed by treatment of with adipogenic inducing agents, resulted in adipocytes with reduced lipid content [18]. This study was different from ours in that the siRNA for Smaf1 was delivered to 3T3-L1 preadipocytes first (rather than at the adipocyte stage as carried out herein); Smaf1 is not expressed in preadipocytes.…”

Section: Sirna-mediated Knockdown Of Smaf1 Does Not Alter Key Aspectsmentioning

confidence: 59%

“…Following our report on the identification of Smaf1, this gene was also reported as adipogenin (Adig) by Hong and coworkers. In that study it was identified via public database mining for adipose-enriched transcripts [18]. However their study also did not provide information as to the nature of the endogenous Smaf1 gene product.…”

Section: Introductionmentioning

confidence: 99%

Expression, regulation and functional assessment of the 80 amino acid Small Adipocyte Factor 1 (Smaf1) protein in adipocytes

Ren

Eskandari

Wang

et al. 2016

Archives of Biochemistry and Biophysics

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“…The HCV-related lipid deregulation causes overexpression of different hepatic enzymes: hormone sensitive Lipase (LIPE), lipoprotein lipase (LPL) and Leptin [15]. Accordingly, patients exhibit serum lipid abnormalities, such as low levels of: LDL [16,17], Resistin (RETN) [18], Adiponectin (ADIPOQ) [19] and Adipogenin (ADIG) [20]. The genes involved in the lipid de novo synthesis and beta oxidation, such as the nuclear receptor Liver X Receptor alpha (LXR alpha), the Sterol regulatory element binding transcription factor 1 (SREBP1c), the Fatty acid synthase (FASN) and the Acetyl CoA carboxylase Beta (ACACB) respectively, are associated with HCV infection, too [21], as well as Fatty acid binding protein 4 (FABP4) that modulates inflammatory and metabolic response that is mainly expressed in adipocytes and macrophages [22].…”

Section: Introductionmentioning

confidence: 99%

Lymphocytes as liver damage mirror of HCV related adipogenesis deregulation

Minutolo¹,

Conti²,

Viscomi³

et al. 2014

Digestive and Liver Disease

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Hepatitis C virus infection leads to a wide spectrum of liver diseases ranging from mild chronic hepatitis to end-stage cirrhosis and hepatocellular carcinoma. An intriguing aspect of the HCV infection is its close connection with lipid metabolism playing an important role in the HCV life cycle and in its pathogenesis. HCV is known to be a hepatotropic virus; however, it can also infect peripheral blood mononuclear cells (PBMCs). The goal of the current investigation is to compare the adipogenesis profile of liver tissues to lymphocytes of HCV infected patients, in order to understand if PBMCs may reflect the alterations of intracellular pathways occurring during HCV-related liver steatosis. Using the Human Adipogenesis PCR Array, gene expression was analyzed in liver samples and PBMCs of chronic HCV+, HBV+ and Healthy Donors (HDs) patients. We observed a similar modulation of lipid metabolism in HCV+ and HBV+liver tissues and lymphoid, cells suggesting that PBMCs reflect the liver adipogenesis deregulation related to infection, even if the two viruses have a different impact in the regulation of the adipogenesis mechanisms. In particular, some genes involved in lipid metabolism and inflammation, as well as in cell transformation, were up-regulated, in a similar way, in both HCV models analyzed. Interestingly, these genes were positively correlated to virological and hepatic functional parameters of HCV+ patients. On the contrary, HBV+ patients displayed a completely different profile. PBMCs of HCV+ patients seem to be useful model to study how HCV-related lipid metabolism deregulation occurs in liver. The obtained data suggest some molecules as new possible biomarkers of HCV-related liver damage progression.

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Up-regulation of adipogenin, an adipocyte plasma transmembrane protein, during adipogenesis

Cited by 30 publications

References 23 publications

Adipose Stromal Cell Tubule Network Model Provides a Versatile Tool for Vascular Research and Tissue Engineering

Adipose Stromal Cell Tubule Network Model Provides a Versatile Tool for Vascular Research and Tissue Engineering

Expression, regulation and functional assessment of the 80 amino acid Small Adipocyte Factor 1 (Smaf1) protein in adipocytes

Lymphocytes as liver damage mirror of HCV related adipogenesis deregulation

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