{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T03:46:27Z","timestamp":1790048787520,"version":"4.0.1"},"reference-count":57,"publisher":"Bioscientifica","issue":"3","license":[{"start":{"date-parts":[[2017,6,1]],"date-time":"2017-06-01T00:00:00Z","timestamp":1496275200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2017,6]]},"abstract":"<jats:p>\n                    We have previously demonstrated that neutrophil recruitment to the heart following myocardial infarction (MI) is enhanced in mice lacking 11\u03b2-hydroxysteroid dehydrogenase type 1 (11\u03b2-HSD1) that regenerates active glucocorticoid within cells from intrinsically inert metabolites. The present study aimed to identify the mechanism of regulation. In a mouse model of MI, neutrophil mobilization to blood and recruitment to the heart were higher in 11\u03b2-HSD1-deficient (\n                    <jats:italic>Hsd11b1<\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\/<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    ) relative to wild-type (WT) mice, despite similar initial injury and circulating glucocorticoid. In bone marrow chimeric mice, neutrophil mobilization was increased when 11\u03b2-HSD1 was absent from host cells, but not when absent from donor bone marrow-derived cells. Consistent with a role for 11\u03b2-HSD1 in \u2018host\u2019 myocardium, gene expression of a subset of neutrophil chemoattractants, including the chemokines\n                    <jats:italic>Cxcl2<\/jats:italic>\n                    and\n                    <jats:italic>Cxcl5<\/jats:italic>\n                    , was selectively increased in the myocardium of\n                    <jats:italic>Hsd11b1<\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\/<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice relative to WT. SM22\u03b1-Cre directed disruption of\n                    <jats:italic>Hsd11b1<\/jats:italic>\n                    in smooth muscle and cardiomyocytes had no effect on neutrophil recruitment. Expression of\n                    <jats:italic>Cxcl2<\/jats:italic>\n                    and\n                    <jats:italic>Cxcl5<\/jats:italic>\n                    was elevated in fibroblast fractions isolated from hearts of\n                    <jats:italic>Hsd11b1<\/jats:italic>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    <jats:sup>\/<\/jats:sup>\n                    <jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                    <\/jats:italic>\n                    mice post MI and provision of either corticosterone or of the 11\u03b2-HSD1 substrate, 11-dehydrocorticosterone, to cultured murine cardiac fibroblasts suppressed IL-1\u03b1-induced expression of\n                    <jats:italic>Cxcl2<\/jats:italic>\n                    and\n                    <jats:italic>Cxcl5<\/jats:italic>\n                    . These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11\u03b2-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.\n                  <\/jats:p>","DOI":"10.1530\/joe-16-0501","type":"journal-article","created":{"date-parts":[[2017,5,18]],"date-time":"2017-05-18T20:20:11Z","timestamp":1495138811000},"page":"315-327","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":33,"title":["11\u03b2-HSD1 suppresses cardiac fibroblast CXCL2, CXCL5 and neutrophil recruitment to the heart post MI"],"prefix":"10.1530","volume":"233","author":[{"given":"Katie J","family":"Mylonas","sequence":"first","affiliation":[{"name":"1University\/BHF Centre for Cardiovascular ScienceUniversity of Edinburgh, Queen\u2019s Medical Research 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