{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T08:24:15Z","timestamp":1780475055559,"version":"3.54.1"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2015,3,8]],"date-time":"2015-03-08T00:00:00Z","timestamp":1425772800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Granulocyte\u2010colony stimulating factor (G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>) has been shown to promote mobilization of bone marrow\u2010derived stem cells (<jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>s) into the bloodstream associated with improved survival and cardiac function after myocardial infarction. Therefore, the aim of the present study was to investigate whether G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> is able to attenuate cardiac remodelling in a mouse model of pressure\u2010induced <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> hypertrophy focusing on mobilization and migration of <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>s. <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> hypertrophy was induced by transverse aortic constriction (<jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content>) in C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6J mice. Four\u00a0weeks after <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> procedure. Mice were treated with G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> (100\u00a0\u03bcg\/kg\/day; Amgen Biologicals) for 2\u00a0weeks. The number of migrated <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>s in the heart was analysed by flow cytometry. <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression and protein level of different growth factors in the myocardium were investigated by <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>. Functional analyses assessed by echocardiography and immunohistochemical analysis were performed 8\u00a0weeks after <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> procedure. G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>\u2010treated animals revealed enhanced homing of <jats:styled-content style=\"fixed-case\">VLA<\/jats:styled-content>\u20104<jats:sup>+<\/jats:sup> and c\u2010kit<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>s associated with increased <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression and protein level of the corresponding homing factors Vascular cell adhesion protein 1 and Stem cell factor in the hypertrophic myocardium. Functionally, G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> significantly preserved <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> function after <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> procedure, which was associated with a significantly reduced area of fibrosis compared to control animals. Furthermore, G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content>\u2010treated animals revealed a significant improvement of survival after <jats:styled-content style=\"fixed-case\">TAC<\/jats:styled-content> procedure. In summary, G\u2010<jats:styled-content style=\"fixed-case\">CSF<\/jats:styled-content> treatment preserves cardiac function and is able to diminish cardiac fibrosis after induction of <jats:styled-content style=\"fixed-case\">LV<\/jats:styled-content> hypertrophy associated with increased homing of <jats:styled-content style=\"fixed-case\">VLA<\/jats:styled-content>\u20104<jats:sup>+<\/jats:sup> and c\u2010kit<jats:sup>+<\/jats:sup> <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>s and enhanced expression of their respective homing factors <jats:styled-content style=\"fixed-case\">VCAM<\/jats:styled-content>\u20101 and <jats:styled-content style=\"fixed-case\">SCF<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/jcmm.12494","type":"journal-article","created":{"date-parts":[[2015,3,9]],"date-time":"2015-03-09T03:08:59Z","timestamp":1425870539000},"page":"1033-1041","source":"Crossref","is-referenced-by-count":10,"title":["Attenuation of cardiac hypertrophy by 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