select ad.sno,ad.journal,ad.title,ad.author_names,ad.abstract,ad.abstractlink,j.j_name,vi.* from articles_data ad left join journals j on j.journal=ad.journal left join vol_issues vi on vi.issue_id_en=ad.issue_id where ad.sno_en='33563' and ad.lang_id='10' and j.lang_id='10' and vi.lang_id='10' Cardiomyocyte-specific Estrogen Receptor Alpha Increases Ang | 33563
ஜர்னல் ஆஃப் செல் சயின்ஸ் & தெரபி

ஜர்னல் ஆஃப் செல் சயின்ஸ் & தெரபி
திறந்த அணுகல்

ஐ.எஸ்.எஸ்.என்: 2157-7013

சுருக்கம்

Cardiomyocyte-specific Estrogen Receptor Alpha Increases Angiogenesis,Lymphangiogenesis and Reduces Fibrosis in the Female Mouse Heart Post-Myocardial Infarction

Shokoufeh Mahmoodzadeh, Joachim Leber, Xiang Zhang, Frédéric Jaisser, Smail Messaoudi, Ingo Morano, Priscilla A Furth, Elke Dworatzek and Vera Regitz- Zagrosek

Experimental 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, LV volume and cardiomyocyte length. 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 only in female ERα-OE after MI. In conclusion, our 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 cardiac remodelling.

மறுப்பு: இந்த சுருக்கமானது செயற்கை நுண்ணறிவு கருவிகளைப் பயன்படுத்தி மொழிபெயர்க்கப்பட்டது மற்றும் இன்னும் மதிப்பாய்வு செய்யப்படவில்லை அல்லது சரிபார்க்கப்படவில்லை.
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