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However, excessive activation of microglia contributes to neurodegenerative diseases. Corticosteroids are potent modulators of inflammation and mediate their effects by binding to mineralocorticoid receptors (MR) and glucocorticoid receptors (GR). Here, the coordinated activities of GR and MR on the modulation of the nuclear factor-\u03baB (NF-\u03baB) pathway in murine BV-2 microglial cells were studied.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>BV-2 cells were treated with different corticosteroids in the presence or absence of MR and GR antagonists. The impact of the glucocorticoid-activating enzyme 11\u03b2-hydroxysteroid dehydrogenase type 1 (11\u03b2-HSD1) was determined by incubating cells with 11-dehydrocorticosterone, with or without selective inhibitors. Expression of interleukin-6 (IL-6), tumor necrosis factor receptor 2 (TNFR2), and 11\u03b2-HSD1 mRNA was analyzed by RT-PCR and IL-6 protein expression by ELISA. NF-\u03baB activation and translocation upon treatment with various corticosteroids were visualized by western blotting, immunofluorescence microscopy, and translocation assays.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>GR and MR differentially regulate NF-\u03baB activation and neuroinflammatory parameters in BV-2 cells. By converting inactive 11-dehydrocorticosterone to active corticosterone, 11\u03b2-HSD1 essentially modulates the coordinated action of GR and MR. Biphasic effects were observed for 11-dehydrocorticosterone and corticosterone, with an MR-dependent potentiation of IL-6 and tumor necrosis factor-\u03b1 (TNF-\u03b1) expression and NF-\u03baB activation at low\/moderate concentrations and a GR-dependent suppression at high concentrations. The respective effects were confirmed using the MR ligand aldosterone and the antagonist spironolactone as well as the GR ligand dexamethasone and the antagonist RU-486. NF-\u03baB activation could be blocked by spironolactone and the inhibitor of NF-\u03baB translocation Cay-10512. Moreover, an increased expression of TNFR2 was observed upon treatment with 11-dehydrocorticosterone and aldosterone, which was reversed by 11\u03b2-HSD1 inhibitors and\/or spironolactone and Cay-10512.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>A tightly coordinated GR and MR activity regulates the NF-\u03baB pathway and the control of inflammatory mediators in microglia cells. The balance of GR and MR activity is locally modulated by the action of 11\u03b2-HSD1, which is upregulated by pro-inflammatory mediators and may represent an important feedback mechanism involved in resolution of inflammation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/1742-2094-9-260","type":"journal-article","created":{"date-parts":[[2012,11,28]],"date-time":"2012-11-28T06:14:25Z","timestamp":1354083265000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":137,"title":["Mineralocorticoid and glucocorticoid receptors differentially regulate NF-kappaB activity and pro-inflammatory cytokine production in murine BV-2 microglial cells"],"prefix":"10.1186","volume":"9","author":[{"given":"Boonrat","family":"Chantong","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise V","family":"Kratschmar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lyubomir G","family":"Nashev","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zoltan","family":"Balazs","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex","family":"Odermatt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2012,11,28]]},"reference":[{"key":"743_CR1_743","doi-asserted-by":"publisher","first-page":"182","DOI":"10.1016\/j.bbrc.2012.01.139","volume":"419","author":"A Hirata","year":"2012","unstructured":"Hirata A, Maeda N, Nakatsuji H, Hiuge-Shimizu A, Okada T, Funahashi T, Shimomura I: Contribution of glucocorticoid-mineralocorticoid receptor pathway on the obesity-related adipocyte dysfunction. \n                           Biochem Biophys Res Commun 2012, 419:182\u2013187.","journal-title":"Biochem Biophys Res Commun"},{"key":"743_CR2_743","doi-asserted-by":"publisher","first-page":"E930","DOI":"10.1152\/ajpendo.00320.2009","volume":"298","author":"T Ishii-Yonemoto","year":"2010","unstructured":"Ishii-Yonemoto T, Masuzaki H, Yasue S, Okada S, Kozuka C, Tanaka T, Noguchi M, Tomita T, Fujikura J, Yamamoto Y, Ebihara K, Hosoda K, Nakao K: Glucocorticoid reamplification within cells intensifies NF-kappaB and MAPK signaling and reinforces inflammation in activated preadipocytes. \n                           Am J Physiol Endocrinol Metab 2010, 298:E930-E940.","journal-title":"Am J Physiol Endocrinol Metab"},{"key":"743_CR3_743","doi-asserted-by":"publisher","first-page":"281","DOI":"10.1016\/j.mce.2011.09.011","volume":"350","author":"V Marzolla","year":"2012","unstructured":"Marzolla V, Armani A, Zennaro MC, Cinti F, Mammi C, Fabbri A, Rosano GM, Caprio M: The role of the mineralocorticoid receptor in adipocyte biology and fat metabolism. \n                           Mol Cell Endocrinol 2012, 350:281\u2013288.","journal-title":"Mol Cell Endocrinol"},{"key":"743_CR4_743","first-page":"269","volume":"19","author":"ER De Kloet","year":"1998","unstructured":"De Kloet ER, Vreugdenhil E, Oitzl MS, Joels M: Brain corticosteroid receptor balance in health and disease. \n                           Endocr Rev 1998, 19:269\u2013301.","journal-title":"Endocr Rev"},{"key":"743_CR5_743","doi-asserted-by":"publisher","first-page":"173","DOI":"10.1016\/0022-4731(84)90380-7","volume":"21","author":"ER De Kloet","year":"1984","unstructured":"De Kloet ER, Veldhuis HD, Wagenaars JL, Bergink EW: Relative binding affinity of steroids for the corticosterone receptor system in rat hippocampus. \n                           J Steroid Biochem Mol Biol 1984, 21:173\u2013178.","journal-title":"J Steroid Biochem Mol Biol"},{"key":"743_CR6_743","doi-asserted-by":"publisher","first-page":"2505","DOI":"10.1210\/endo-117-6-2505","volume":"117","author":"JM Reul","year":"1985","unstructured":"Reul JM, de Kloet ER: Two receptor systems for corticosterone in rat brain: microdistribution and differential occupation. \n                           Endocrinology 1985, 117:2505\u20132511.","journal-title":"Endocrinology"},{"key":"743_CR7_743","doi-asserted-by":"publisher","first-page":"459","DOI":"10.1677\/joe.0.1150459","volume":"115","author":"JM Reul","year":"1987","unstructured":"Reul JM, van den Bosch FR, de Kloet ER: Relative occupation of type-I and type-II corticosteroid receptors in rat brain following stress and dexamethasone treatment: functional implications. \n                           J Endocrinol 1987, 115:459\u2013467.","journal-title":"J Endocrinol"},{"key":"743_CR8_743","first-page":"55","volume":"21","author":"RM Sapolsky","year":"2000","unstructured":"Sapolsky RM, Romero LM, Munck AU: How do glucocorticoids influence stress responses? 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