Basic fibroblast growth factor messenger ribonucleic acid levels in human placentas from normal and pathological pregnancies

被引:14
作者
Di Blasio, AM
Carniti, C
Vigano, P
Florio, P
Petraglia, F
Vignali, M
机构
[1] Ist Auxol Italiano Milano, Mol Biol Lab, I-20135 Milan, Italy
[2] Univ Milan, Dept Obstet & Gynecol 2, Milan, Italy
[3] Univ Pisa, Dept Obstet & Gynecol, Pisa, Italy
关键词
basic fibroblast growth factor; basic fibroblast growth factor receptor; diabetes; placenta;
D O I
10.1093/molehr/3.12.1119
中图分类号
Q [生物科学];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
This study was designed to determine whether basic fibroblast growth factor (bFGF) gene expression in human placenta varies as a function of gestational age and to evaluate whether bFGF synthesis might be altered in pathological pregnancies. Moreover, we also investigated whether human placental cells express the bFGF receptor gene, The presence of mRNA for bFGF and its receptor was demonstrated by reverse transcriptase-polymerase chain reaction (RT-PCR) performed on total RNA derived from human placental cells at different times of culture, Levels of bFGF mRNA were determined by competitive RT-PCR in human placental tissues collected at the beginning and at the end of pregnancy, Competitive RT-PCR was also employed to evaluate bFGF synthesis in term placentas derived from pregnancies complicated by diabetes. mRNA for both bFGF and its receptor were demonstrated in human placenta starting as early as 8 weeks of pregnancy. Values of bFGF mRNA were significantly higher in first trimester compared with term placentas. Term placentas derived from pregnancies associated with type I diabetes expressed levels of bFGF mRNA higher than those present in normal term placentas. These data demonstrate that bFGF and its receptor are synthesized in human placental cells throughout gestation. Moreover, bFGF gene expression is developmentally regulated. Finally, bFGF might also be partially responsible for the placental alterations observed in pregnancies complicated by diabetes.
引用
收藏
页码:1119 / 1123
页数:5
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