title: Differential regulation of cardiac protein kinase C isozyme expression after aortic banding in rat.
abstract: OBJECTIVE
  Protein kinase C (PKC) plays a key role in myocardial hypertrophy. To evaluate whether its isoforms are expressed differentially during gradual development of pressure-overload-induced cardiac hypertrophy, banding of the ascending aorta was used as an experimental model of left ventricular hypertrophy.
  
  
  METHODS
  One, 7 and 30 days after sham operation or aortic banding in male Wistar rats, the PKC activity and the expression of the cardiac PKC isozymes (PKC-alpha, -delta, - epsilon and -zeta), both at the protein and the mRNA level, were determined in the left and right ventricle.
  
  
  RESULTS
  Left ventricular hypertrophy developed rapidly as early as 1 day after aortic banding followed by further progression at day 7 and day 30. This was paralleled by an increased total PKC enzyme activity in the cytosol fraction and a selectively enhanced protein expression of PKC-delta (day 7, 267+/-18%; day 30, 289+/-12%) and PKC-alpha (day 7, 212+/-20%; day 30, 193+/-14%). The protein amount of PKC- epsilon was not changed in either group. This differential protein expression was associated with a significant increase of the absolute mRNA levels for PKC-delta and PKC-alpha up to 202+/-20% (day 30) and 177+/-17% (day 30), whereas significant alterations in the PKC- epsilon mRNA levels were not detected. A selective upregulation of PKC-alpha and PKC-delta, both on the protein and on the mRNA level, was also noted in the right ventricle during the development of right ventricular hypertrophy, suggesting an adaptive response following elevated left ventricular enddiastolic pressure after long-term aortic banding for 30 days.
  
  
  CONCLUSIONS
  This study characterizes in the right and left ventricle a differential regulation of the dominant PKC isozymes in pressure-overload cardiac hypertrophy both at the protein and the mRNA level.
authors.affiliation: Department of Cardiology, Medical Clinic II, University of Technology Dresden, Fetscherstr. 76, Dresden, Germany.
authors.forename: Martin U
authors.initials: MU
authors.lastname: Braun
authors.forename: Paul
authors.initials: P
authors.lastname: LaRosée
authors.forename: Steffen
authors.initials: S
authors.lastname: Schön
authors.forename: Mathias M
authors.initials: MM
authors.lastname: Borst
authors.forename: Ruth H
authors.initials: RH
authors.lastname: Strasser
mesh_terms: D000818:Animals; D015153:Blotting, Western / Q000379:methods; D003600:Cytosol / Q000201:enzymology; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000201:enzymology*; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D023421:Models, Animal; D009206:Myocardium / Q000201:enzymology*; D009638:Norepinephrine / Q000097:blood; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013347:Subcellular Fractions / Q000201:enzymology
chemical_list: D007527:Isoenzymes; D012333:RNA, Messenger; D011493:Protein Kinase C; D009638:Norepinephrine