کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2790173 | 1568581 | 2006 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IGFBP1 and Follistatin-like 3 Genes are Significantly Up-regulated in Expression Profiles of the IUGR Placenta
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی تکاملی
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چکیده انگلیسی
To date, the clinicopathological features of intrauterine growth restriction (IUGR) are not clearly understood, and no effective therapy has been established for IUGR. This is the first study that uses microarray analysis to identify differentially expressed genes in the IUGR placenta. The expression profiles of a total of 9121 genes were examined by cDNA microarray analysis, using mRNA from an appropriate gestational age (AGA) placenta and an IUGR placenta from discordant dichorionic twins. Up-regulation of the IGFBP1 and Follistatin-like 3 genes was detected in the IUGR placenta, with a balanced differential degree of 20.7 ± 1.3 and 13.1 ± 2.1, respectively, while the balanced differential degrees of other genes were 2.6 or less. The expressions of the IGFBP1 and Follistatin-like 3 genes in four single IUGR and four AGA placentas were also examined by RT-PCR. Consistent with our data in discordant chorionic twin placentas, three of four IUGR placentas showed up-regulation of the IGFBP1 and all four IUGR placentas showed upregulation of Follistatin-like 3 genes when compared to the AGA placentas. Our results suggest that IGFBP1 and Follistatin-like 3 are highly up-regulated in IUGR in the placenta. IGFBP1 and Follistatin-like 3 are known critical regulators of fetal growth and differentiation. Pathways associated with these genes might be important for the pathogenesis of IUGR.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Placenta - Volume 27, Issues 2â3, FebruaryâMarch 2006, Pages 317-321
Journal: Placenta - Volume 27, Issues 2â3, FebruaryâMarch 2006, Pages 317-321
نویسندگان
A. Okamoto, H. Endo, B. Kalionis, M. Shinya, M. Saito, T. Nikaido, T. Tanaka,