Estrogen and Progesterone Modulate Monocyte Cell Cycle Progression and Apoptosis

Thongngarm, Torpong; Jenkins, John K.; Ndebele, Kenneth; McMurray, Robert W.

doi:10.1034/j.1600-0897.2003.00015.x

Cited by 47 publications

(27 citation statements)

References 33 publications

(50 reference statements)

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“…There is evidence that pregnancy-related hormones have a specific inhibitory effect on monocyte cell cycle progression and induce their apoptosis. 28 Thus, birth removes the source of myeloid cell suppression and may allow the growth of a pre-established lesion, possibly explaining the observed perinatal growth of these tumors. Circulating maternal angiogenesis inhibitors have also been described during pregnancy, which is another idea that should be considered as a mechanism for the perinatal onset of hemangiomas.…”

Section: Discussionmentioning

confidence: 99%

Myeloid Cells in Infantile Hemangioma

Ritter

Reinisch

Friedlander

et al. 2006

The American Journal of Pathology

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Little is known about the pathogenesis of infantile hemangiomas despite the fact that they are relatively common tumors. These benign neoplasms occur in as many as 1 in 10 births, and although rarely life threatening, hemangiomas can pose serious concerns to the cosmetic and psychosocial development of the afflicted child. Ulceration, scarring, and disfigurement are significant problems as are encroachment of the ear and eye, which can threaten hearing and vision. The precise mechanisms controlling the rapid growth observed in the first months of life and the spontaneous involution that follows throughout the course of years remain unknown. In this report we demonstrate the presence of large numbers of hematopoietic cells of the myeloid lineage in proliferating hemangiomas and propose a mechanism for the observed evolution of these lesions that is triggered by hypoxia and involves the participation of myeloid cells. We report the results of experiments using myeloid markers (CD83, CD32, CD14, CD15) that unexpectedly colabeled hemangioma endothelial cells, providing new evidence that these cells are distinct from normal endothelium.

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Section: Discussionmentioning

confidence: 99%

Myeloid Cells in Infantile Hemangioma

Ritter

Reinisch

Friedlander

et al. 2006

The American Journal of Pathology

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“…While evidence for the direct regulation of macrophage proliferation by estrogens is lacking, these hormones were shown to modulate bone marrow M-CSF production and reduced aortic expression of M-CSF was found in Apoe-deficient mice treated with E 2 (Sarma et al 1998, Lea et al 1999, Martin-McNulty et al 2003. E 2 was also demonstrated to promote apoptosis of monocytes, monocyte-derived macrophages, and macrophage-derived osteoclasts, and these effects were largely attributed to the upregulation of Fas and Fas ligand (FasL (FASLG)) as well as the activity of caspases 8 and 3 (Carruba et al 2003, Mor et al 2003, Thongngarm et al 2003, Saintier et al 2006, Nakamura et al 2007, Montagna et al 2009). In this context, it is worth noting that Fas/FasL effectively regulate apoptosis of cholesterol-loaded macrophages and that Fas and FasL-mediated macrophage apoptosis coincides with decreased lesion cellularity and regression of atherosclerosis in mice (Esaki et al 2000, Yao & Tabas 2000.…”

Section: Involvement Of Macrophages Dendritic Cells and Lymphocytesmentioning

confidence: 99%

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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“…Bei Frauen in der Menopause sinkt die Zahl der Monozyten wieder, wenn sie sich einer Östrogener-satztherapie unterziehen. Erklärt wird dieser Effekt durch die Induktion eines mitotischen Arrests oder von Apoptose in Monozyten durch Östrogen und Progesteron [12].…”

Section: Monozytenunclassified

Frauen und Autoimmunerkrankungen mit vaskulärer und (peri)kardialer Beteiligung

Portig

Sandmöller²,

Pankuweit³

et al. 2005

Herz

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Women's greater susceptibility to autoimmune diseases has been recognized for more than 100 years. And although the basic immune response (including a more vigorous immune response and increased antibody production) has been known to differ between men and women, conclusive pathophysiological explanations for this phenomenon are still lacking. Experimental work done in animal models have revealed a profound influence of sex hormones on the susceptibility to autoimmune diseases and on clinical disease via direct and indirect signaling pathways. Apart from sex hormones additional factors seem to participate in the pathogenesis of autoimmune diseases, which remain to be elucidated ("so far, you cannot explain autoimmunity [only] with estrogen" [lockshin]).

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Estrogen and Progesterone Modulate Monocyte Cell Cycle Progression and Apoptosis

Cited by 47 publications

References 33 publications

Myeloid Cells in Infantile Hemangioma

Myeloid Cells in Infantile Hemangioma

Estrogens and atherosclerosis: insights from animal models and cell systems

Frauen und Autoimmunerkrankungen mit vaskulärer und (peri)kardialer Beteiligung

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