期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：39
页码：14234-14239
DOI：10.1073/pnas.0405571101
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Although the heart responds to estrogen, it is not clear whether estrogen acts directly on heart muscle or indirectly by means of the vascular, immune, or nervous system. No role for estrogen receptor (ER) {beta} in the heart has been established, but ER{beta}-/- mice are hypertensive, and as they age, their hearts become enlarged. Histological and ultrastructural analysis of the heart revealed a disarray of myocytes, a disruption of intercalated discs, an increase in the number and size of gap junctions, and a profound alteration in nuclear structure, concomitantly with a loss of expression of lamin A/C from the nuclear envelope. In the lungs of ER{beta}-/- mice, lamin A/C was located in the nuclear membrane, indicating that lamin A/C is not an ER{beta}-regulated gene. Immunohistochemical studies with ER{beta} antibodies failed to detect ER{beta} in the myocardium. We conclude that abnormalities in heart morphology in ER{beta}-/- mice are likely due to stress on the nuclear envelope as a result of the chronic sustained systolic and diastolic hypertension observed in ER{beta}-/- mice. Because neither ER{alpha} nor ER{beta} could be detected in heart muscle, the effects of estrogen on the myocardium seem to be indirect.
