title: Scar and pulmonary expression and shedding of ACE in rat myocardial infarction.
abstract: We examined the topology of angiotensin-converting enzyme (ACE) mRNA expression, activity, and shedding in myocardial infarction-induced heart failure and sought to elucidate the source of the increased plasma ACE activity in this model. Three months after coronary ligature, lung, scar, and remaining viable left ventricular tissues were analyzed for ACE mRNA expression as well as tissue and solubilized ACE activity. ACE mRNA expression increased in the scar with respect to infarct severity, decreased in the lung, and remained unchanged in the left ventricle. ACE activity decreased in the lung and increased in the scar tissue and plasma. Shedding of ACE remained constant in the lung and increased in the scar. This study shows that ACE expression and activity is shifted from the pulmonary endothelium to the infarct scar tissue and that constancy of shedding in the lung and its increase in the scar are the source of the increased plasma ACE in congestive heart failure.
authors.affiliation: Cardiovascular Research Department, Institut National de la Santé et de la Recherche Médicale, 75018 Paris, France.
authors.forename: Roger
authors.initials: R
authors.lastname: Gaertner
authors.forename: Fabrice
authors.initials: F
authors.lastname: Prunier
authors.forename: Monique
authors.initials: M
authors.lastname: Philippe
authors.forename: Liliane
authors.initials: L
authors.lastname: Louedec
authors.forename: Jean-Jacques
authors.initials: JJ
authors.lastname: Mercadier
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Michel
mesh_terms: D000818:Animals; D004151:Dipeptides / Q000494:pharmacology; D004195:Disease Models, Animal; D004452:Echocardiography; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D004789:Enzyme Activation / Q000187:drug effects / Q000502:physiology; D015870:Gene Expression; D006333:Heart Failure / Q000209:etiology / Q000473:pathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008168:Lung / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D009929:Organ Size; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D011480:Protease Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar
chemical_list: D004151:Dipeptides; C078131:N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide; D011480:Protease Inhibitors; D012333:RNA, Messenger; D007703:Peptidyl-Dipeptidase A