Effects of oral and transdermal estrogen therapies on circulating cytokines and chemokines in postmenopausal women with hysterectomy

Saijo, Ayako; Uemura, Hirokazu; Matsuzaki, Takashi; Tsuchiya, Naho; Yuzurihara, Mitsutoshi; Kase, Yoshio; Irahara, Minoru

doi:10.1530/eje-09-0063

Cited by 18 publications

(14 citation statements)

References 36 publications

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“…Although the identity of the RANKL-expressing cells in this latter study was not determined, the cells were in the flowcytometric fraction that contains lymphocytes. Consistent with the idea that B cells may increase in estrogen-deficient women, administration of estradiol or raloxifene to post-menopausal women reduces circulating levels of IL-7 (44,45).…”

Section: Discussionmentioning

confidence: 56%

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

Fujiwara

Piemontese

Liu

et al. 2016

Journal of Biological Chemistry

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Edited by Luke O'NeillThe cytokine receptor activator of NFB ligand (RANKL) produced by osteocytes is essential for osteoclast formation in cancellous bone under physiological conditions, and RANKL production by B lymphocytes is required for the bone loss caused by estrogen deficiency. Here, we examined whether RANKL produced by osteocytes is also required for the bone loss caused by estrogen deficiency. Mice lacking RANKL in osteocytes were protected from the increase in osteoclast number and the bone loss caused by ovariectomy. Moreover, these mice did not exhibit the increase in bone marrow B lymphocytes caused by ovariectomy that occurred in control littermates. Deletion of estrogen receptor ␣ from B cells did not alter B cell number or bone mass and did not alter the response to ovariectomy. In addition, lineage-tracing studies demonstrated that B cells do not act as osteoclast progenitors in estrogen-replete or estrogen-deficient mice. Taken together, these results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the increase in B cell number caused by estrogen deficiency. Moreover, they suggest that estrogen control of B cell number is indirect via osteocytes and that the increase in bone marrow B cells may be a necessary component of the cascade of events that lead to cancellous bone loss during estrogen deficiency. However, the role of B cells is not to act as osteoclast progenitors but may be to act as osteoclast support cells.

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Section: Discussionmentioning

confidence: 56%

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

Fujiwara

Piemontese

Liu

et al. 2016

Journal of Biological Chemistry

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“…Estrogen, specifically E2, is secreted mainly by the ovaries in premenopausal women (Shimizu, 2010). Estrogen circulates in the bloodstream and affects many tissues, including the urogenital system (Yasui et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Estradiol plays a role in regulating the expression of lysyl oxidase family genes in mouse urogenital tissues and human Ishikawa cells

Zong

Jiang

Zhao

et al. 2015

J. Zhejiang Univ. Sci. B

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Abstract:The lysyl oxidase (LOX) family encodes the copper-dependent amine oxidases that play a key role in determining the tensile strength and structural integrity of connective tissues by catalyzing the crosslinking of elastin or collagen. Estrogen may upregulate the expression of LOX and lysyl oxidase-like 1 (LOXL1) in the vagina. The objective of this study was to determine the effect of estrogen on the expression of all LOX family genes in the urogenital tissues of accelerated ovarian aging mice and human Ishikawa cells. Mice and Ishikawa cells treated with estradiol (E2) showed increased expression of LOX family genes and transforming growth factor β1 (TGF-β1). Ishikawa cells treated with TGF-β1 also showed increased expression of LOX family genes. The Ishikawa cells were then treated with either E2 plus the TGF-β receptor (TGFBR) inhibitor SB431542 or E2 alone. The expression of LOX family genes induced by E2 was reduced in the Ishikawa cells treated with TGFBR inhibitor. Our results showed that E2 increased the expression of the LOX family genes, and suggest that this induction may be mediated by the TGF-β signal pathway. E2 may play a role in regulating the expression of LOX family genes.

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“…This may be related to the regulatory effects of estrogen on the production of inflammatory cytokines (Georgiadou & Sbarouni 2009). For instance, an in vivo study showed that transdermal estrogen therapy reduces circulating levels of several cytokines, including MCP-1 (Yasui et al 2009). In parallel, studies in vitro demonstrate that estrogen reduces MCP-1 production in several cells, such as peripheral blood mononuclear cells and immature dendritic cells (Bengtsson et al 2004, Yuan et al 2008).…”

Section: Discussionmentioning

confidence: 99%

17β-estradiol down-regulates lipopolysaccharide-induced MCP-1 production and cell migration in vascular smooth muscle cells

Jiang¹,

Xu²,

Zheng³

et al. 2010

Journal of Molecular Endocrinology

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Atherosclerosis is an inflammatory disease where lipopolysaccharide (LPS) triggers the release of inflammatory cytokines that accelerate its initiation and progression. Estrogen has been proven to be vasoprotective against atherosclerosis; however, the anti-inflammatory function of estrogen in the vascular system remains obscure. In this study, we investigated the effect of estrogen on LPS-induced monocyte chemoattractant protein-1 (MCP-1; listed as CCL2 in the MGI database) production in vascular smooth muscle cells (VSMCs). LPS significantly enhances MCP-1 production and this is dependent on nuclear factor k B (NFkB) signaling, since the use of NFkB inhibitor pyrrolidine dithiocarbamate or the silencing of NFkB subunit p65 expression with specific siRNA largely impairs LPS-enhanced MCP-1 production. On the contrary, 17b-estradiol (E 2 ) inhibits LPS-induced MCP-1 production in a time-and dosedependent manner, which is related to the suppression of p65 translocation to nucleus. Furthermore, p38 MAPK is rapidly activated in response to LPS, while E 2 markedly inhibits p38 MAPK activation. Transfection with p38 MAPK siRNA or the use of p38 MAPK inhibitor SB203580 markedly attenuates LPS-stimulated p65 translocation to nucleus and MCP-1 production, suggesting that E 2 suppresses NFkB signaling by the inactivation of p38 MAPK signaling. LPS promotes VSMCs migration and this is abrogated by MCP-1 antibody, implying that MCP-1 may play a major role as an autocrine factor in atherosclerosis. In addition, E 2 inhibits LPS-promoted cell migration by downregulation of MCP-1 production.Overall, our results demonstrate that E 2 exerts anti-inflammatory property antagonistic to LPS in VSMCs by reducing MCP-1 production, and this effect is related to the inhibition of p38 MAPK/NFkB cascade.

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Effects of oral and transdermal estrogen therapies on circulating cytokines and chemokines in postmenopausal women with hysterectomy

Cited by 18 publications

References 36 publications

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

RANKL (Receptor Activator of NFκB Ligand) Produced by Osteocytes Is Required for the Increase in B Cells and Bone Loss Caused by Estrogen Deficiency in Mice

Estradiol plays a role in regulating the expression of lysyl oxidase family genes in mouse urogenital tissues and human Ishikawa cells

17β-estradiol down-regulates lipopolysaccharide-induced MCP-1 production and cell migration in vascular smooth muscle cells

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