Estrogen and raloxifene inhibit the monocytic chemoattractant protein-1-induced migration of human monocytic cells via nongenomic estrogen receptor α

Yada-Hashimoto, Namiko; Nishio, Yukihiro; Ohmichi, Masahide; Hayakawa, Jun; Mabuchi, Seiji; Hisamoto, Koji; Nakatsuji, Yuki; Sasaki, Hiroshi; Seino-Noda, Hozumi; Sakata, Masahiro; Tasaka, Keiichi; Murata, Yuji

doi:10.1097/01.gme.0000248732.78698.a7

Cited by 17 publications

(12 citation statements)

References 37 publications

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“…Although we adjusted for age and pack-years in the multivariate model, it is uncertain whether adjustment for these covariates is appropriate. Second, although the advantage of only male selection in this study can avoid confrontation in plasma MCP-1 level variation by sex [26,27] and by menopausal status among women [28,29], the results may not be generalizable beyond Taiwanese men. Therefore, the external validity should have a limitation in other population.…”

Section: And Bode Index (Body-mass Index (B) Degree Of Airflow Obstrmentioning

confidence: 64%

MCP1 −2518Polymorphism and chronic obstructive pulmonary disease in Taiwanese men

Liu

Wang

Fang

et al. 2010

Experimental Lung Research

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Monocyte chemoattractant protein-1 (MCP-1) plays a major role in the recruitment of inflammatory cells to the lungs of patients with chronic obstructive pulmonary disease (COPD). However, the influence of MCP1 gene polymorphism on COPD development has not been studied. This study aimed to investigate the association between MCP1 -2518 polymorphisms and COPD and between this polymorphism and plasma MCP-1 levels. The plasma MCP-1 was measured by using an enzyme-linked immunosorbent assay and polymorphisms detection was performed by denaturing high-performance liquid chromatography. COPD group had higher plasma MCP1 levels than healthy participants (257.0 versus 194.4 pg/mL) in the univariate analysis (P = .005); and in stepwise liner regression analysis after adjustment for age, alcohol, body mass index, cancer history, and steroid use (P = .002; 95% confidence interval [CI]: 30.72-128.02). Plasma MCP-1 was negatively correlated with forced expiratory volume in one second (FEV(1)%) (P = .003; r = -.274). SNPStats including codominant, dominant, recessive, overdominant, and log-additive model analysis showed MCP1 -2518 polymorphisms had no association with the risk of COPD. Generalized linear model showed no association between plasma MCP-1 levels and MCP1 -2518 genotypes. In conclusion, there is no association between MCP1 -2518 gene polymorphisms and COPD or between this gene polymorphisms and plasma MCP-1 levels in the Taiwanese men.

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Section: And Bode Index (Body-mass Index (B) Degree Of Airflow Obstrmentioning

confidence: 64%

MCP1 −2518Polymorphism and chronic obstructive pulmonary disease in Taiwanese men

Liu

Wang

Fang

et al. 2010

Experimental Lung Research

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“…Sex and age or HOMA-IR do not influence the net secretion of MCP-1 from adipose tissue [70], but post-menopausal treatment with HRT is associated with a significant decrease in circulating MCP-1 [72]. Estrogen is a negative regulator of the MCP-1 gene activation [73], and in THP-1 cells, estrogen inhibits MCP-1-induced monocyte migration [74]. The production of MIF from in vitro cultured s.c. and omental preadipocytes and adipocytes is positively associated with BMI, with no difference between the depots [75].…”

Section: Inflammationmentioning

confidence: 99%

Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism

Mattsson¹,

Olsson

2007

CMC

118

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Women have a higher percentage of body fat than men, and there is a gender-specific difference in fat distribution: Females tend to accumulate fat around the hips, buttocks, and thighs while men have a larger intra-abdominal (visceral) fat mass. After menopause, there is a redistribution of fat depots, and post-menopausal women develop increased amounts of visceral fat. The risk of developing obesity-related diseases is significantly lower in pre-menopausal women compared to men, a difference that is abolished after menopause, suggesting that the female sex steroid estrogen influences adipogenesis and adipose metabolism. Experimentally, estrogen increases the size and number of subcutaneous adipocytes and attenuates lipolysis. Post-menopausal women also develop a more atherogenic lipid pattern and decreased levels of the prothrombotic protein plasminogen activator inhibitor-1, which attenuates fibrinolysis. Pathologically increased circulating cortisol concentration is associated with dysmetabolic features e.g., central obesity, elevated blood pressure, insulin resistance, and dyslipidemia. In "simple obesity," glucocorticoid production is elevated. Peak levels of circulating cortisol are however low or normal, possibly because of increased clearance and/or tissue-specific changes in cortisol production. In addition to the adrenal production of cortisol, cortisol is also generated in adipose tissue by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) which converts inactive cortisone to active cortisol. The enzyme activity in subcutaneous fat increases with increasing body weight. Estrogen seems to have a tissue-specific influence on 11betaHSD1 enzyme activity, attenuating it in liver, kidney, and testis but upregulating 11betaHSD1 mRNA expression in preadipocytes from women. In the present review, we summarize and discuss the interaction between glucocorticoids and sex steroids and their influence on adipocyte metabolism.

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“…(Álvarez, Hermenegildo, Issekutz, Esplugues, & Sanz, 2002) Estrogen inhibited MCP-1 induced migration of THP-1 cells. (Yada-Hashimoto et al, 2006) The utilization of HUVECs as a model for many of these studies limits applicability of the results, as it is becoming increasingly apparent that HUVECs differ significantly in their responses from endothelial cells derived from adult arteries. (Tan et al, 2004; Lucas, Rose, & Morris, 2000)…”

Section: Atherosclerosismentioning

confidence: 99%

Estrogen and the cardiovascular system

Knowlton

Lee

2012

Pharmacology & Therapeutics

340

224

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Estrogen is a potent steroid with pleiotropic effects, which have yet to be fully elucidated. Estrogen has both nuclear and non-nuclear effects. The rapid response to estrogen, which involves a membrane associated estrogen receptor(ER) and is protective, involves signaling through PI3K, Akt, and ERK 1/2. The nuclear response is much slower, as the ER-estrogen complex moves to the nucleus, where it functions as a transcription factor, both activating and repressing gene expression. Several different ERs regulate the specificity of response to estrogen, and appear to have specific effects in cardiac remodeling and the response to injury. However, much remains to be understood about the selectivity of these receptors and their specific effects on gene expression. Basic studies have demonstrated that estrogen treatment prevents apoptosis and necrosis of cardiac and endothelial cells. Estrogen also attenuates pathologic cardiac hypertrophy. Estrogen may have great benefit in aging as an anti-inflammatory agent. However, clinical investigations of estrogen have had mixed results, and not shown the clear-cut benefit of more basic investigations. This can be explained in part by differences in study design: in basic studies estrogen treatment was used immediately or shortly after ovariectomy, while in some key clinical trials, estrogen was given years after menopause. Further basic research into the underlying molecular mechanisms of estrogen’s actions is essential to provide a better comprehension of the many properties of this powerful hormone.

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Estrogen and raloxifene inhibit the monocytic chemoattractant protein-1-induced migration of human monocytic cells via nongenomic estrogen receptor α

Abstract: Our findings suggest that both E2 and raloxifene inhibited the MCP-1-induced monocyte migration through nongenomic ERalpha. This result may explain one of the antiatherosclerotic effects of E2 and raloxifene on vasculature.

Cited by 17 publications

References 37 publications

MCP1 −2518Polymorphism and chronic obstructive pulmonary disease in Taiwanese men

MCP1 −2518Polymorphism and chronic obstructive pulmonary disease in Taiwanese men

Estrogens and Glucocorticoid Hormones in Adipose Tissue Metabolism

Estrogen and the cardiovascular system

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