title: Right ventricular upregulation of the Ca(2+) binding protein S100A1 in chronic pulmonary hypertension.
abstract: The Ca(2+) binding protein S100A1 increases the Ca(2+) release from the sarcoplasmatic reticulum by interacting with the ryanodine receptor. In order to understand whether this effect might be operative in the early course of hypertrophy, when myocardium is able to meet increased workload, we investigated the expression of S100A1 in a model of moderate right ventricular hypertrophy. The pulmonary arteries of nine pigs were embolised three times with Sephadex G-50. After 70 days, all pigs showed a moderate pulmonary hypertension. Right ventricular tissue of embolised animals showed a significant increase of connective tissue and enlargement of myocyte diameters. In controls, we found a differential expression of S100A1 with significantly lower S100A1 protein levels in right ventricular compared to left ventricular tissue. In pulmonary hypertension, S100A1 expression increased significantly in hypertrophied right ventricles while it was unchanged in left ventricular tissue. No change was observed in the expression of SERCA2a and phospholamban. Our data show, for the first time, that moderate pressure overload results in an upregulation of S100A1. This may reflect an adaptive response of myocardial Ca(2+) homeostasis to a higher workload.
authors.affiliation: Medizinische Klinik II, Medizinische Universität zu Lübeck, Ratzeburger Allee 160, D-23538, Lübeck, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Ehlermann
authors.forename: A
authors.initials: A
authors.lastname: Remppis
authors.forename: O
authors.initials: O
authors.lastname: Guddat
authors.forename: J
authors.initials: J
authors.lastname: Weimann
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: J
authors.initials: J
authors.lastname: Motsch
authors.forename: C W
authors.initials: CW
authors.lastname: Heizmann
authors.forename: H A
authors.initials: HA
authors.lastname: Katus
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000096:biosynthesis* / Q000235:genetics; D048429:Cell Size; D002908:Chronic Disease; D003911:Dextrans; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D017380:Hypertrophy, Right Ventricular / Q000209:etiology / Q000473:pathology; D017136:Ion Transport; D008297:Male; D011651:Pulmonary Artery; D011655:Pulmonary Embolism / Q000139:chemically induced / Q000150:complications; D009418:S100 Proteins; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D013552:Swine; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
chemical_list: D002135:Calcium-Binding Proteins; D003911:Dextrans; D009418:S100 Proteins; C110294:S100A1 protein; C025614:sephadex; D002118:Calcium