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Cardiomyocyte-specific overexpression of estrogen receptor alpha promotes angiogenesis and lymphangiogenesis and reduces fibrosis in the female mouse heart after myocardial infarction
Zhang, Xiang

HaupttitelCardiomyocyte-specific overexpression of estrogen receptor alpha promotes angiogenesis and lymphangiogenesis and reduces fibrosis in the female mouse heart after myocardial infarction
TitelvarianteKardiomyozyten-spezifischer Überexpression des Östrogen-Rezeptor alpha fördert Angiogenese und Lymphangiogenese sowie reduziert Fibrose in dem weiblichen Mausherz nach Myokardinfarkt.
AutorZhang, Xiang
Geburtsort: Hebei, China
GutachterN.N
weitere GutachterN.N
Freie SchlagwörterEstrogen receptor alpha; myocardial infarction; angiogenesis; lymphangiogenesis; cardiac fibrosis
DDC610 Medizin und Gesundheit
ZusammenfassungExperimental studies showed that 17β-estradiol (E2) and activated estrogen receptors (ER) protect the heart from ischemic injury. However, the underlying molecular mechanisms are not well understood. To investigate the role of ER-alpha (ERα) in cardiomyocytes in the setting of myocardial ischemia, we generated transgenic mice with cardiomyocyte-specific overexpression of ERα (ERα-OE) and subjected them to myocardial infarction (MI). At the basal level, female and male ERα-OE mice showed increased left ventricular (LV) mass and LV volume. Two weeks after MI, LV volume was significantly increased and LV wall thickness decreased in female and male WT-mice and male ERα-OE, but not in female ERα-OE mice. ERα-OE enhanced expression of angiogenesis and lymphangiogenesis markers (VEGF, LYVE-1), and neovascularization in the peri-infarct area in both sexes. However, attenuated level of fibrosis and higher phosphorylation of JNK signaling pathway could be detected in only female ERα-OE after MI. In conclusion, this study indicates that ERα protects female mouse cardiomyocytes from the sequelae of ischemia through induction of neovascularization in a paracrine fashion and impaired fibrosis, which together may contribute to the attenuation of the adverse consequence of cardiac remodeling.
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Seitenzahl63
Fachbereich/EinrichtungMedizinische Fakultät Charité - Universitätsmedizin Berlin
Erscheinungsjahr2015
Dokumententyp/-SammlungenDissertation
Medientyp/FormatText
SpracheEnglisch
Rechte Nutzungsbedingungen
Tag der Disputation30.05.2015
Erstellt am07.05.2015 - 11:46:15
Letzte Änderung03.08.2015 - 10:50:16
 
Statische URLhttp://edocs.fu-berlin.de/diss/receive/FUDISS_thesis_000000098795
URNurn:nbn:de:kobv:188-fudissthesis000000098795-4
Zugriffsstatistik
E-Mail-Adressexiang820312@gmail.com