The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Myeloid-specific estrogen receptor α deficiency impairs metabolic homeostasis and accelerates atherosclerotic lesion development
Open accessAbstract
ERα is expressed in macrophages and other immune cells known to exert dramatic effects on glucose homeostasis. We investigated the impact of ERα expression on macrophage function to determine whether hematopoietic or myeloid-specific ERα deletion manifests obesity-induced insulin resistance in mice. Indeed, altered plasma adipokine and cytokine levels, glucose intolerance, insulin resistance, and increased adipose tissue mass were observed in animals harboring a hematopoietic or myeloid-specific deletion of ERα. A similar obese phenotype and increased atherosclerotic lesion area was displayed in LDL receptor-KO mice transplanted with ERα −/− bone marrow. In isolated macrophages, ERα was necessary for repression of inflammation, maintenance of oxidative metabolism, IL-4–mediated induction of alternative activation, full phagocytic capacity in response to LPS, and oxidized LDL-induced expression of ApoE and Abca1. Furthermore, we identified ERα as a direct regulator of macrophage transglutaminase 2 expression, a multifunctional atheroprotective enzyme. Our findings suggest that diminished ERα expression in hematopoietic/myeloid cells promotes aspects of the metabolic syndrome and accelerates atherosclerosis in female mice.
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Cites
Inflammation and metabolic disorders
Hotamisligil, G. S. (2006) · Nature · doi:10.1038/nature05485 · Cited by 9,199
Obesity induces a phenotypic switch in adipose tissue macrophage polarization
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Inflammation, stress, and diabetes
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Estrogen Resistance Caused by a Mutation in the Estrogen-Receptor Gene in a Man
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Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
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“Alternative macrophage activation is associated with antiinflammatory actions, wound healing, and a lean mouse phenotype (25, 35, 36).”
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IKK-β links inflammation to obesity-induced insulin resistance
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Self-citationNormalization of obesity-associated insulin resistance through immunotherapy
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Oxidative metabolism and PGC-1β attenuate macrophage-mediated inflammation
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“(35) linking inflammation with cellular oxidative metabolism, we observed a 47% (P = 0.”
Background
Cited by
The role of estrogens in control of energy balance and glucose homeostasis
Mauvais-Jarvis, F., Clegg, D. J., & Hevener, A. L. (2013) · Endocrine Reviews · doi:10.1210/er.2012-1055 · Cited by 1,329
Self-citationEstrogen receptors regulate innate immune cells and signaling pathways
Kovats, S. (2015) · Cellular Immunology · doi:10.1016/j.cellimm.2015.01.018 · Cited by 984
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training
Roberts, C. K., Hevener, A. L., & Barnard, R. J. (2013) · Comprehensive Physiology · doi:10.1002/cphy.c110062 · Cited by 831
Self-citationMacrophage phenotypes in atherosclerosis
Colin, S., Chinetti‐Gbaguidi, G., & Staels, B. (2014) · Immunological Reviews · doi:10.1111/imr.12218 · Cited by 657
The pathophysiology of hypertension in patients with obesity
DeMarco, V. G., Aroor, A. R., & Sowers, J. R. (2014) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2014.44 · Cited by 545
Metadata
- Authors
- Ribas, V., Drew, B. G., Le, J. A., Soleymani, T., Daraei, P., Sitz, D., Mohammad, L., Henstridge, D. C., Febbraio, M. A., Hewitt, S. C., Korach, K. S., Bensinger, S. J., & Hevener, A. L.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-09-07
- Volume
- 108
- Issue
- 39
- Pages
- 16457-16462
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2037725361
- Cited by
- 181
- References
- 19
- FWCI
- 9.51
- Type
- journal article
- Language
- en
- Open access
- green
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- Ribas, V., Drew, B. G., Le, J. A., Soleymani, T., Daraei, P., Sitz, D., Mohammad, L., Henstridge, D. C., Febbraio, M. A., Hewitt, S. C., Korach, K. S., Bensinger, S. J., & Hevener, A. L. (2011). Myeloid-specific estrogen receptor α deficiency impairs metabolic homeostasis and accelerates atherosclerotic lesion development. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1104533108
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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