先兆子痫患者胎盘中生长因子受体结合蛋白2表达上调提示ras信号的可能作用

来源 :世界核心医学期刊文摘(妇产科学分册) | 被引量 : 0次 | 上传用户:LQ0121
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Objectives: To screen for genes with altered expression in placentas from pregnancies complicated by preeclampsia. Study design: To corroborate gene expression profile of preeclamptic and normal placentas (ATLASTM Clontech), by dot blot, Northern blot analysis and RT- PCR for growth factor receptor bound- protein 2 (GRB2), using immunohistochemistry to localize its expression in the placenta. Results: Increased expression of GRB2 upregulated in the microarrays was found in preeclampsia by Dot blot and Northern blot analysis. RT- PCR performed with primers specific for GRB2 and its alternatively spliced isoform GRB3- 3 showed that most of the cDNA represented in the array was GRB2. The protein was localized to the smooth muscle wall of stem vessels by immunohistochemistry. Conclusion:The ras signalling activated by placental receptor tyrosine kinases may play a role in the segmental thickening of the stem vascular wall in preeclamptic placentas, resulting in reduced blood flow to the developing fetus. Objectives: To screen for genes with altered expression in placentas from pregnancies complicated by preeclampsia. Study design: To corroborate gene expression profile of preeclamptic and normal placentas (ATLASTM Clontech), by dot blot, Northern blot analysis and RT-PCR for growth factor receptor bound-protein 2 (GRB2), using immunohistochemistry to localize its expression in the placenta. Results: Increased expression of GRB2 upregulated in the microarrays was found in preeclampsia by Dot blot and Northern blot analysis. RT-PCR performed with primers specific for GRB2 and Its alternatively spliced ​​isoform GRB3-3 showed that most of the cDNA represented in the array was GRB2. The protein was localized to the smooth muscle wall of stem vessels by immunohistochemistry. Conclusion: The ras signaling activated by placental receptor tyrosine kinases may play a role in the segmental thickening of the stem vascular wall in preeclamptic placentas, resulting in reduced blood flow to the de veloping fetus.
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