Inhibition of Transplant Coronary Arteriosclerosis in Rabbits by Chronic Estradiol Treatment Is Associated With Abolition of MHC Class II Antigen Expression

Lou, Hong; Kodama, Teruaki; Zhao, Ye Jun; Maurice, P; Wang, Yi Ning; Katz, Nevin M.; Foegh, Marie L.

doi:10.1161/01.cir.94.12.3355

Cited by 59 publications

(35 citation statements)

References 29 publications

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“…Similarly, both E 2 and synthetic ER agonists normalized NF-kB activation and pro-inflammatory cytokine production as well as reduced TLR4 expression in Kupfer cells following trauma-hemorrhage in rats and mice, and these effects were shown to be specifically mediated by ERa (Hsieh et al 2007, Suzuki et al 2007. In addition, transplant arteriosclerosis in rats or rabbits as well as macrophage infiltration into the allograft intima were potently reduced in E 2 -treated recipients, and this was associated with almost complete suppression of MHC-II antigen expression in transplanted arteries (Lou et al 1996, Saito et al 1998. Most recently, ERa-deficient macrophages were found refractory to IL4-induced activation of anti-inflammatory phenotype in vitro and presented with elevated expression of chemokines and markers of immune cell activity, when isolated from animals with myeloid-specific ERa deficiency (Ribas et al 2011).…”

Section: Involvement Of Macrophages Dendritic Cells and Lymphocytesmentioning

confidence: 89%

Estrogens and atherosclerosis: insights from animal models and cell systems

Nofer

2012

Journal of Molecular Endocrinology

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Estrogens not only play a pivotal role in sexual development but are also involved in several physiological processes in various tissues including vasculature. While several epidemiological studies documented an inverse relationship between plasma estrogen levels and the incidence of cardiovascular disease and related it to the inhibition of atherosclerosis, an interventional trial showed an increase in cardiovascular events among postmenopausal women on estrogen treatment. The development of atherosclerotic lesions involves complex interplay between various pro-or anti-atherogenic processes that can be effectively studied only in vivo in appropriate animal models. With the advent of genetic engineering, transgenic mouse models of atherosclerosis have supplemented classical dietary cholesterolinduced disease models such as the cholesterol-fed rabbit. In the last two decades, these models were widely applied along with in vitro cell systems to specifically investigate the influence of estrogens on the development of early and advanced atherosclerotic lesions. The present review summarizes the results of these studies and assesses their contribution toward better understanding of molecular mechanisms underlying anti-and/or pro-atherogenic effects of estrogens in humans.

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Section: Involvement Of Macrophages Dendritic Cells and Lymphocytesmentioning

confidence: 89%

Estrogens and atherosclerosis: insights from animal models and cell systems

Nofer

2012

Journal of Molecular Endocrinology

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“…Furthermore, Foegh et al demonstrated that estrogens ameliorate transplant arteriosclerosis in cardiac and aortic allografts [6,18,191. The role of estrogens, however, in the development of renal disease is controversial.…”

Section: Discussionmentioning

confidence: 99%

Opposite effects of testosterone and estrogens on chronic allograft nephropathy

et al. 2002

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In the present study we investigated whether donor gender or the effects of sex hormones play the greater role in the development of chronic allograft nephropathy. Kidneys of male and female Fisher rats were orthotopically transplanted into castrated male Lewis recipients. Animals were treated with testosterone, estradiol, or vehicle and the kidneys were harvested 20 weeks after transplantation for histological, immunohistological, and molecular analysis. Testosterone treatment resulted in increased proteinuria and profound glomerulosclerosis, irrespective of donor gender. In addition, mRNA levels of transforming growth factor-PI (TGF-01) and platelet-derived growth factor-A and B (PDGF-A and B) chains were enhanced in these allografts. Estradiol reduced glomerulosclerosis and mononuclear cell infiltration in allografts of both genders that paralleled a decreased mRNA expression of TGF-P1, PDGF-A and B. No donor genderrelated differences were noted in vehicle-treated animals. Our findings demonstrate that sex hormones rather than donor gender have a significant impact on chronic allograft nephropathy.

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“…The current study does not answer this question, as we did not observe the expression of PDGF-B and other growth factors that are thought to be involved in the development of GCA. 30 Further studies on these issues are needed to clarify possible mechanisms underlying the effects of PDGF-A and other growth factors on cardiac grafts.…”

Section: Discussionmentioning

confidence: 99%