کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1984466 1539975 2007 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Temporal expression pattern of Bardet-Biedl syndrome genes in adipogenesis
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Temporal expression pattern of Bardet-Biedl syndrome genes in adipogenesis
چکیده انگلیسی

Bardet-Biedl syndrome (BBS) is an autosomal recessive disorder associated with marked obesity. Research in rare forms of obesity has identified genes with significant roles in common obesity etiology. To date, 11 BBS genes have been cloned (BBS1–BBS11). However, the function of BBS genes in adipogenesis is unknown. Moreover, not all BBS genes have been shown to be expressed in adipose tissue. The aim of our study was to investigate the expression of BBS genes throughout adipogenesis. 3T3-F442A preadipocyte cells were harvested throughout the adipogenesis process (from day 1 to 8) at 1-day intervals. Levels of BBS genes transcripts were analyzed by quantitative real-time polymerase chain reaction (PCR). Additionally, transcript levels of BBS5–9 and BBS11 were studied in mouse (C57BL/6) adipose tissue. We have shown for the first time that BBS5–9 and BBS11 are expressed in adipose tissue. Significant variations in the transcript levels of the BBS genes were identified throughout adipogenesis. Compared to the their levels in non-differentiated preadipocytes, transcript levels of BBS1–4, 6–9 and 11 were significantly augmented through differentiation, reaching maximum values at day 3 (BBS1–4, 6–8) and 4 (BBS9 and 11) by 3.5, 4, 2.9, 3, 5, 1.9, 2, 2.9 and 2.6-fold, respectively.These findings show for the first time a unique, temporal and synchronized expression of BBS genes during adipogenesis. These findings highlight the importance of BBS genes functional studies in adipogenesis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 39, Issue 5, 2007, Pages 1055–1062
نویسندگان
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