2005年3月
RNA interference of PPAR gamma using fiber-modified adenovirus vector efficiently suppresses preadipocyte-to-adipocyte differentiation in 3T3-L1 cells
GENE
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- 巻
- 348
- 号
- 開始ページ
- 157
- 終了ページ
- 165
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.gene.2005.01.005
- 出版者・発行元
- ELSEVIER SCIENCE BV
The peroxisome proliferator-activated receptor (PPAR) gamma is regarded as a "master regulator" of adipocyte differentiation and is abundantly expressed in adipose. To understand the biological role of PPAR gamma in adipose, RNA interference (RNAi) of PPAR gamma should be a powerful tool. 3T3-L1 cell line serves an excellent model to investigate the mechanism of preadipocyte-to-adipocyte differentiation. However, this cell line is difficult to transfect by plasmid vectors and viral vectors. We optimized the transduction of both 3T3-L1 preadipocytes and adipocytes by means of fiber-modified adenovirus (Ad) vectors. Among the various vectors tested, polylysine modification of the C-terminal of the fiber knob most markedly improved the transduction efficiency in both 3T3-L1 preadipocytes and adipocytes. Then, we examined whether fiber-modified Ad vectors with polylysine peptides expressing the small interfering RNA (siRNA) for PPAR gamma inhibit the differentiation of 3T3-L1 preadipocytes into adipocytes. Oil red 0 staining and measurement of glycerol-3-phosphate dehydrogenase (GPDH) activity indicated that the vectors effectively suppressed the differentiation of 3T3-L1 preadipocytes to adipocytes. These results suggested that the combination of fiber-modified Ad vectors containing polylysine peptides and RNAi is an effective tool for the study of the biological and physiological mechanism of adipogenesis in adiposity and diabetes using 3T3-L1 models. Ad vector-mediated RNAi for PPAR gamma should also be useful to clarify the biological role of the PPAR gamma pathway in various tissues in addition to adipose and for therapeutic application to a variety of diseases, including adiposity and diabetes. (c) 2005 Elsevier B.V. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.gene.2005.01.005
- ISSN : 0378-1119
- Web of Science ID : WOS:000228318700016