Circulating chemoattractants RANTES, negatively related to endogenous androgens, and MCP-1 are differentially suppressed by hormone therapy and raloxifene

Christodoulakos, George; Lambrinoudaki, Ιrene; Economou, Emmanuel; Papadias, C.; Vitoratos, N.; Panoulis, Constantinos; Kouskouni, Evangelia; Vlachou, Sofia; Creatsas, George

doi:10.1016/j.atherosclerosis.2006.05.045

Cited by 20 publications

(15 citation statements)

References 78 publications

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“…Taken together, it could be possible that the sexual dimorphic nature of p38 could influence SAA-induced Ccl2 expression in female mice but not males in our study. In addition, there is some evidence that estrogen confers some protection against high fat diet-induced systemic and adipose tissue inflammation [52], [53], which could contribute to reduced Ccl2 expression [54], [55]. Lower baseline Ccl2 expression in the gWAT of female chow-fed Saa3 +/+ mice compared to their male counterparts supports this notion.…”

Section: Discussionmentioning

confidence: 89%

Deletion of Serum Amyloid A3 Improves High Fat High Sucrose Diet-Induced Adipose Tissue Inflammation and Hyperlipidemia in Female Mice

et al. 2014

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Serum amyloid A (SAA) increases in response to acute inflammatory stimuli and is modestly and chronically elevated in obesity. SAA3, an inducible form of SAA, is highly expressed in adipose tissue in obese mice where it promotes monocyte chemotaxis, providing a mechanism for the macrophage accumulation that occurs with adipose tissue expansion in obesity. Humans do not express functional SAA3 protein, but instead express SAA1 and SAA2 in hepatic as well as extrahepatic tissues, making it difficult to distinguish between liver and adipose tissue-specific SAA effects. SAA3 does not circulate in plasma, but may exert local effects that impact systemic inflammation. We tested the hypothesis that SAA3 contributes to chronic systemic inflammation and adipose tissue macrophage accumulation in obesity using mice deficient for Saa3 (Saa3 −/−). Mice were rendered obese by feeding a pro-inflammatory high fat, high sucrose diet with added cholesterol (HFHSC). Both male and female Saa3 −/− mice gained less weight on the HFHSC diet compared to Saa3+/+ littermate controls, with no differences in body composition or resting metabolism. Female Saa3 −/− mice, but not males, had reduced HFHSC diet-induced adipose tissue inflammation and macrophage content. Both male and female Saa3 −/− mice had reduced liver Saa1 and Saa2 expression in association with reduced plasma SAA. Additionally, female Saa3 −/− mice, but not males, showed improved plasma cholesterol, triglycerides, and lipoprotein profiles, with no changes in glucose metabolism. Taken together, these results suggest that the absence of Saa3 attenuates liver-specific SAA (i.e., SAA1/2) secretion into plasma and blunts weight gain induced by an obesogenic diet. Furthermore, adipose tissue-specific inflammation and macrophage accumulation are attenuated in female Saa3 −/− mice, suggesting a novel sexually dimorphic role for this protein. These results also suggest that Saa3 influences liver-specific SAA1/2 expression, and that SAA3 could play a larger role in the acute phase response than previously thought.

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Section: Discussionmentioning

confidence: 89%

Deletion of Serum Amyloid A3 Improves High Fat High Sucrose Diet-Induced Adipose Tissue Inflammation and Hyperlipidemia in Female Mice

et al. 2014

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“…Dihydrotestosterone has also been shown to decrease tumor necrosis factor-a and lipopolysaccharide-induced inflammatory response in human endothelial cells (33). Furthermore, endogenous androgens in postmenopausal women have been reported to correlate negatively with circulating regulated upon activation, normal T-cell expressed and secreted (RANTES), a potent chemoattractant of T-lymphocytes (34). In addition, testosterone has been found to have direct vasodilatory effects initiated at the smooth muscle cell membrane of the endothelium, which contains testosterone binding sites (35).…”

Section: Discussionmentioning

confidence: 99%

Endogenous sex hormone levels in postmenopausal women undergoing carotid artery endarterectomy

Debing¹,

Peeters²,

Duquet³

et al. 2007

eur j endocrinol

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Objective: To study the endogenous sex hormone levels in natural postmenopausal women and their association with the presence of internal carotid artery (ICA) atherosclerosis. Design: Case-control study Methods: We compared 56 patients with severe ICA atherosclerosis referred for carotid artery endarterectomy (CEA) with 56 age-matched control subjects free of severe atherosclerotic disease. The presence of atherosclerosis was determined by high-resolution B-mode ultrasound. Metabolic parameters and sex hormones were measured or calculated: total cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides, glucose, insulin, quantitative insulin sensitivity check index, insulin resistance index, IGF-I, DHEA, DHEA sulfate (DHEA-S), free testosterone, total testosterone, estrone, estradiol, androstenedione, and sex hormone-binding globulin. Results: The cases had statistically significant lower levels of both total testosterone (0.23G0.12 vs 0.31G0.20 mg/l, PZ0.043) and free testosterone (3.42G1.94 vs 4.59G2.97 ng/l, PZ0.009) and significantly lower levels of androstenedione (625.3G168.7 vs 697.0G211.9 ng/l, PZ0.017) when compared with controls. Multivariate linear regression analysis, adjusted for traditional cardiovascular risk factors, baseline and physiologic characteristics, showed a significant inverse relationship between both serum free testosterone (bZK0.234, PZ0.028) and androstenedione (bZK0.241, PZ0.028) levels with the presence of severe atherosclerosis of ICA. Conclusions:The study provides evidence of a positive association between low serum androgen levels and severe ICA atherosclerosis in postmenopausal women. It suggests that higher, but physiological, levels of androgens in postmenopausal women have a protective role in the development of atherosclerosis of ICA.European Journal of Endocrinology 156 687-693

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“…RANTES targets several subpopulations of lymphocytes. Both IL-16 and RANTES have been implicated previously in other autoimmune diseases (Klimiuk et al, 1999;Simchen et al, 2000) and elevated levels of both have been detected in the general circulation of patients with chronic inflammatory disease (Blaschke et al, 2001;Christodoulakos et al, 2007).…”

Section: B Graves' Diseasementioning

confidence: 96%

Insulin-Like Growth Factor-I Regulation of Immune Function: A Potential Therapeutic Target in Autoimmune Diseases?

2010

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Circulating chemoattractants RANTES, negatively related to endogenous androgens, and MCP-1 are differentially suppressed by hormone therapy and raloxifene

Cited by 20 publications

References 78 publications

Deletion of Serum Amyloid A3 Improves High Fat High Sucrose Diet-Induced Adipose Tissue Inflammation and Hyperlipidemia in Female Mice

Deletion of Serum Amyloid A3 Improves High Fat High Sucrose Diet-Induced Adipose Tissue Inflammation and Hyperlipidemia in Female Mice

Endogenous sex hormone levels in postmenopausal women undergoing carotid artery endarterectomy

Insulin-Like Growth Factor-I Regulation of Immune Function: A Potential Therapeutic Target in Autoimmune Diseases?

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