Expression of Liver-Type Fatty-Acid-Binding Protein, Fatty Acid Synthase and Vascular Endothelial Growth Factor in Human Lung Carcinoma

Pathobiology ◽  
2005 ◽  
Vol 72 (5) ◽  
pp. 233-240 ◽  
Author(s):  
Tetsuo Kawamura ◽  
Ryuzo Kanno ◽  
Hiroshi Fujii ◽  
Toshimitsu Suzuki
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Fatty Acid Binding Protein ◽  
Human Lung ◽  
Vascular Endothelial ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Human Lung Carcinoma ◽  
Endothelial Growth Factor

scholarly journals RNA Interference-Based Silencing Reveals the Regulatory Role of Fatty Acid-Binding Protein 4 in the Production of IL-6 and Vascular Endothelial Growth Factor in 3T3-L1 Adipocytes

Endocrinology ◽  
2012 ◽  
Vol 153 (11) ◽  
pp. 5629-5636 ◽  
Author(s):  
Kazuaki Kajimoto ◽  
Shiharu Takayanagi ◽  
Shun Sasaki ◽  
Hidetaka Akita ◽  
Hideyoshi Harashima
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Adipose Tissue ◽  
Growth Factor ◽  
Small Interfering Rna ◽  
Fatty Acid Binding Protein ◽  
Vascular Endothelial ◽  
Fatty Acid Binding ◽  
Acid Binding Protein ◽  
Interfering Rna ◽  
Endothelial Growth Factor

Abstract The fatty acid-binding protein 4 (FABP4) is believed to play an important role in maintaining glucose and lipid homeostasis. However, the physiological functions of FABP4 in adipocytes have not been fully elucidated because of difficulties associated with the effective transfection of small interfering RNA (siRNA) to differentiated adipocytes. The aim of this study was to clarify the physiological roles of FABP4 in adipocytes by establishing an efficient, universal technique for endogenous gene silencing in fully differentiated 3T3-L1 cells. Confocal-based three-dimensional observations demonstrated that, in traditionally cultured 3T3-L1 cells, multilayers of undifferentiated cells were formed. As a result, small interfering RNA failed to reach many of the differentiated cells. To solve this problem, we developed a reliable method, denoted as density-based separation followed by replating of enriched adipocytes in a monolayer (DREAM) and, using the developed method, succeeded in a significant knockdown of FABP4. Loss-of-function analyses revealed that FABP4 regulates the expression of IL-6 and vascular endothelial growth factor (VEGF) mediated by the protease-activated receptor 1 (PAR1), a thrombin receptor, in adipocytes. In addition, the basal IL-6 production was partially suppressed by PAR1 knockdown. Moreover, we also demonstrated that IL-6 stimulates the proliferation of primary endothelial cells isolated from murine adipose tissue. These findings indicate that FABP4 may have a crucial role in modulating IL-6 and vascular endothelial growth factor as angiogenesis inducers stimulated by the cellular action of thrombin on adipocytes via PAR1. These findings promise to be helpful for developing an understanding of physiological counterparts with respect to the inflammatory and angiogenic properties of adipose tissue.

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