| Hu CM |
------>authors3_c= ------>paper_class1=1 ------>Impact_Factor=14.595 ------>paper_class3=2 ------>paper_class2=1 ------>vol=110 ------>confirm_bywho=sylin ------>insert_bywho=sunpowerhu ------>Jurnal_Rank=1.3 ------>authors4_c= ------>comm_author= ------>patent_EDate=None ------>authors5_c= ------>publish_day=1 ------>paper_class2Letter=None ------>page2=316 ------>medlineContent= ------>unit=E0125 ------>insert_date=20090917 ------>iam=1 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN= ------>authors_c= ------>score=500 ------>journal_name=Circulation ------>paper_name=Heme oxygenase-1 inhibits angiotensin II-induced cardiac hypertrophy in vitro and in vivo ------>confirm_date=20090918 ------>tch_id=098012 ------>pmid=15226216 ------>page1=309 ------>fullAbstract=BACKGROUND: Heme oxygenase-1 (HO-1) is a stress-response enzyme implicated in cardioprotection. To explore whether HO-1 has a role in cardiac remodeling response, the effect of its overexpression on angiotensin II (Ang II)-induced cardiac hypertrophy was examined. METHODS AND RESULTS: HO-1 was induced in cultured rat neonatal cardiomyocytes by treatment with cobalt protoporphyrin IX (CoPPIX) or a recombinant adenovirus carrying the human HO-1 gene. Ang II-induced myocyte hypertrophy assessed by increments in cell size, [3H]leucine uptake, and protein content was suppressed by HO-1 overexpression. Cotreatment of cells with tin protoporphyrin IX, a HO inhibitor, significantly reversed the suppressive effect of HO-1. Bilirubin, one of the byproducts of heme degradation by HO-1, mediated the suppressive effect through the inhibition of Ang II-induced production of reactive oxygen species, as detected by a 2~,7~-dichlorofluorescein probe. The antihypertrophic effect of HO-1 was also demonstrated in rats receiving chronic Ang II infusions. Cotreatment of animals with CoPPIX significantly attenuated Ang II-induced left ventricular hypertrophy and hyperdynamic contractions, whereas concomitant treatment with tin protoporphyrin IX abolished CoPPIX-mediated cardioprotection in vivo. CONCLUSIONS: HO-1 attenuates Ang II-induced cardiac hypertrophy both in vitro and in vivo, and bilirubin mediates, at least in part, the antihypertrophic effect of HO-1 via inhibition of reactive oxygen species production after Ang II stimulation. ------>tmu_sno=None ------>sno=22195 ------>authors2=Chen YH ------>authors3=Chiang MT ------>authors4=Chau LY ------>authors5= ------>authors6= ------>authors6_c= ------>authors=Hu CM ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c= ------>publish_area=0 ------>updateTitle=Heme oxygenase-1 inhibits angiotensin II-induced cardiac hypertrophy in vitro and in vivo. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2004 ------>submit_flag=None ------>publish_month=1 |