Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts

Kovacs, Elizabeth J.; Faunce, Douglas E.; Ramer-Quinn, D S; Mott, Francis J.; Dy, Peter; Frazier-Jessen, Michelle R.

doi:10.1002/jlb.59.4.562

Cited by 33 publications

(19 citation statements)

References 29 publications

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“…AP-1 has recently been characterized as an antioxidant-responsive transcription factor. 32,33 Estradiolinduced decreases in MCP-1 mRNA expression 12,14 as well as increases in NO synthase expression 34 have been assumed to be mediated in part by estrogen receptor (ER)␣, because tamoxifen, an ER␣ receptor antagonist, attenuates these effects. However, it is possible that part of the effect of estradiol on the vessel wall may be mediated by the newly discovered ER␤, as it has recently been demonstrated that after carotid arterial injury in a mouse model in which the ER␣ gene is disrupted, estradiol inhibited vascular smooth muscle cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…However, a direct inhibitory action of estradiol on MCP-1 production in macrophages has also been demonstrated by other investigators. [12][13][14]16 Potential mechanisms by which estradiol may inhibit MCP-1 expression must also be considered. For example, NO inhibits MCP-1 gene expression 27 and estradiol increases NO production in endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…Estradiol inhibits JE/MCP-1 mRNA expression in murine macrophages induced by lipopolysaccharide 12 and talc, 13 as well as in platelet-derived growth factor-induced murine fibroblasts. 14 The inhibitory effect of estradiol on MCP-1 mRNA expression led to the speculation that the antiatherogenic effects of estradiol may be mediated by the prevention of macrophage accumulation in the atherosclerotic area. 12 Estradiol in addition inhibited the migration of human monocytes stimulated with either MCP-1 15 or minimally oxidized LDL 16 in vitro.…”

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confidence: 99%

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Estradiol Suppresses MCP-1 Expression In Vivo

Pervin

Singh

Rosenfeld

et al. 1998

ATVB

116

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Abstract-The mechanisms by which 17␤-estradiol retards atherogenesis are not known. The adhesion of monocytes to endothelial cells followed by the migration of monocytes into the artery wall are key cellular events that occur throughout the entire atherogenic process and may be responsive to estradiol. Monocyte chemoattractant protein-1 (MCP-1), a chemokine that is expressed in atherosclerotic lesions, is thought to play a major role in stimulating the migration of blood monocytes into developing atherosclerotic lesions. We therefore assessed the effects of estradiol in vivo on MCP-1 protein and mRNA expression in the descending thoracic aorta of rabbits fed a cholesterol-enriched (0.5%) diet for 6 weeks and in animals fed normal chow. MCP-1 protein was quantified by Western blot analysis and monocyte chemotaxis bioassay, and reverse transcription-polymerase chain reaction was used to ascertain the level of MCP-1 mRNA expression. We observed that in both ovary-intact and ovariectomized (OVX) animals, MCP-1 protein and mRNA expression were significantly increased by 6 weeks in animals fed a high-cholesterol diet. The cholesterol-induced increase in MCP-1 protein and mRNA expression was significantly attenuated in OVX rabbits supplemented with estradiol pellets (1.5-and 10.0-mg 60-day-release pellets), which yielded a range of estradiol concentrations encompassing the physiological levels. MCP-1 protein and mRNA expression were increased in normocholesterolemic OVX rabbits compared with normocholesterolemic ovary-intact animals, and this increase was prevented in OVX animals supplemented with estradiol pellets.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Estradiol Suppresses MCP-1 Expression In Vivo

Pervin

Singh

Rosenfeld

et al. 1998

ATVB

116

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“…In addition, several studies in animals show full atheroprotection at E2 doses that do not alter the lipid profile (2). Thus attention has focused on the direct effects of E2 on the vessel wall and on the processes involved in the inflammatory and fibroproliferative components of atherosclerosis including: endothelial permeability to LDL (10), LDL oxidation (11,12), cytokine and cell adhesion molecule expression (13)(14)(15)(16), macrophage cholesterol homeostasis (17), vascular smooth muscle cell and neointimal proliferation and migration (18,19), calcification (20,21) and platelet adhesion and aggregation (22).…”

Section: Introductionmentioning

confidence: 99%

Estrogen receptor α is a major mediator of 17β-estradiol’s atheroprotective effects on lesion size in Apoe–/– mice

Hodgin¹,

Krege²,

Reddick³

et al. 2001

J. Clin. Invest.

207

141

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The inhibitory effects of estrogen (17β-estradiol) on atherosclerosis have been well documented in numerous animal models, and epidemiological evidence supports this protective effect in humans. The detailed mechanisms for this protection are not understood, but most are thought to be mediated through estrogen receptors (ERs), of which two are known (ERα and ERβ). To investigate the role of ERα in the atheroprotective effect of 17β-estradiol (E2), we ovariectomized female mice that lack apoE (AAee) or lack both apoE and ERα (ααee), and treated half of them with E2 for three months. E2 treatment of ovariectomized AAee females dramatically reduced the size of the lesions as well as their histological complexity. Plasma cholesterol was significantly reduced in this group, although the observed extent of protection by E2 was greater than could be explained solely by the change in lipid levels. In contrast, E2 treatment of ovariectomized ααee females caused minimal reduction in lesion size and no reduction in total plasma cholesterol compared with ααee mice without E2, demonstrating that ERα is a major mediator of the atheroprotective effect of E2. Nevertheless, E2 treatment significantly reduced the complexity of plaques in the ααee females, although not to the same degree as in AAee females, suggesting the existence of ERα-independent atheroprotective effects of E2.

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“…Finally, neither of the bone resorption inhibitory hormones, calcitonin or 17␤-estradiol, directly influenced either basal or IL-1␣-stimulated IL-8 release from hOCL, although hOCL expressed mRNA for each receptor and have responded in other ways to calcitonin (46) and 17␤-estradiol (47). Estrogen also does not affect basal or stimulated IL-8 release by hBMS, hOB, or human MG-63 osteosarcoma cells (19,48,49), although estrogen can inhibit cytokine-induced MCP-1 production in fibroblasts (50). Thus, hOCL production of IL-8 is predominantly regulated by inflammatory mediators and not by other osteotropic factors or hormones.…”

Section: Discussionmentioning

confidence: 89%

Human Osteoclasts and Osteoclast-Like Cells Synthesize and Release High Basal and Inflammatory Stimulated Levels of the Potent Chemokine Interleukin-8¹

et al. 1998

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Chemokines, including interleukin-8 (IL-8), function as key mediators in diverse inflammatory disorders via promoting the recruitment, proliferation, and activation of vascular and immune cells. IL-8 levels are elevated in inflammatory diseases, such as rheumatoid arthritis, osteoarthritis, osteomyelitis, and periodontal disease, that also exhibit progressive bone loss. Therefore, it is possible that IL-8 contributes to the osteopenia associated with these pathological conditions. Although macrophages, neutrophils, and endothelial cells are considered the primary sources of inflammation-induced IL-8 increases, we report here for the first time that human bone marrowderived osteoclast-like cells (hOCL) as well as authentic bone-resorbing human osteoclasts (hOC) isolated from osteoporotic femoral heads express messenger RNA (mRNA) for IL-8 and secrete high levels of IL-8 during culture. Basal IL-8 release by cultured hOC or hOCL was orders of magnitude greater than the release of the proinflammatory cytokines IL-1␤, IL-6, and tumor necrosis factor-␣. At a cellular level, in situ hybridization analysis revealed that IL-8 mRNA was expressed in resorbing hOC of rheumatoid arthritic pannus and was substantially greater than that expressed in hOC of noninflammatory giant cell tumor of bone tissue. Therefore, the potential inflammationmediated induction of IL-8 was directly assessed using cultured hOCL. IL-8 release was stimulated by proinflammatory signals (IL-1␣, tumor necrosis factor-␣, lipopolysaccharide, or phorbol 12-myristate 13-acetate), unaffected by various other osteotropic modulators (transforming growth factor-␤1 and -␤3, IL-6, 17␤-estradiol, or calcitonin) and was decreased by interferon-␥, vitamin D 3 , and the antiinflammatory glucocorticoid dexamethasone. Changes in IL-8 secretion were paralleled by corresponding changes in IL-8 mRNA steady state levels. We conclude that hOC and hOCL synthesize and secrete high constitutive and inflammation-stimulated levels of the chemokine IL-8. Consequently, hOC-derived IL-8 could act as an important regulatory signal for bone, vascular, and immune cell recruitment and activation during normal and pathological bone remodeling. (Endocrinology 139: [4353][4354][4355][4356][4357][4358][4359][4360][4361][4362][4363] 1998)

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Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts

Cited by 33 publications

References 29 publications

Estradiol Suppresses MCP-1 Expression In Vivo

Estradiol Suppresses MCP-1 Expression In Vivo

Estrogen receptor α is a major mediator of 17β-estradiol’s atheroprotective effects on lesion size in Apoe–/– mice

Human Osteoclasts and Osteoclast-Like Cells Synthesize and Release High Basal and Inflammatory Stimulated Levels of the Potent Chemokine Interleukin-8¹

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Estrogen regulation of JE/MCP-1 mRNA expression in fibroblasts

Cited by 33 publications

References 29 publications

Estradiol Suppresses MCP-1 Expression In Vivo

Estradiol Suppresses MCP-1 Expression In Vivo

Estrogen receptor α is a major mediator of 17β-estradiol’s atheroprotective effects on lesion size in Apoe–/– mice

Human Osteoclasts and Osteoclast-Like Cells Synthesize and Release High Basal and Inflammatory Stimulated Levels of the Potent Chemokine Interleukin-81

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Human Osteoclasts and Osteoclast-Like Cells Synthesize and Release High Basal and Inflammatory Stimulated Levels of the Potent Chemokine Interleukin-8¹