Increased maternal cortisol in late-gestation ewes decreases fetal cardiac expression of 11beta-HSD2 mRNA and the ratio of AT1 to AT2 receptor mRNA.
Increased maternal cortisol in late-gestation ewes decreases fetal cardiac expression of 11beta-HSD2 mRNA and the ratio of AT1 to AT2 receptor mRNA.
复制标题
妊娠晚期母羊母体皮质醇增加会降低胎儿心脏 11β-HSD2 mRNA 的表达以及 AT1 与 AT2 受体 mRNA 的比率。
DOI：
10.1152/ajpregu.00294.2006
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Keller-Wood,Maureen
中科院分区：
文献类型：
--
作者：
Reini,SethA;Wood,CharlesE;Jensen,Ellen;Keller-Wood,Maureen
Moderately elevated maternal cortisol levels late in gestation cause enlargement of the fetal sheep heart. We have used quantitative real-time PCR to examine expression of candidate genes in fetal hearts from mothers in whom cortisol levels were increased (by infusion of 1 mg cortisol·kg−1·day−1) or decreased (by adrenalectomy and replacement to 0.5 mg cortisol·kg−1·day−1) from 115 to 130 days gestation. Control ewes were not treated with steroid. Expression of mineralocorticoid receptor (MR), glucocorticoid receptor (GR), 11β-hydroxysteroid dehydrogenases 1 and 2 (11β-HSD1 and -2), IGF I and II, IGF receptors 1 and 2 (IGF-1R and IGF-2R), endothelial nitric oxide synthase, VEGF, myotrophin, angiotensinogen, the angiotensin receptors 1 and 2 (AT1R and AT2R), and the angiotensin converting enzymes 1 and 2 were measured. MR mRNA abundance in fetal hearts was found to be similar to that in adult kidney and hippocampus. Although there were no significant changes in most genes, 11β-HSD2 and IGF-1R expression were significantly decreased in the high cortisol group and 11β-HSD2 expression negatively correlated to left ventricular wall thickness. There was also a significant change in the ratio of AT receptor expression, with increased AT2R and decreased AT1R in the high cortisol group. MR, GR, and 11β-HSD1 immunoreactivity was found in cardiomyocytes and cardiac blood vessels in 126–128 day fetal sheep; in contrast 11β-HSD2 staining was predominantly in blood vessels. These results indicate that cortisol could indeed act in the fetal heart to induce enlargement and suggest that the renin-angiotensin system may play a role.
