RGD Reference Report - Cardiac function and remodeling is attenuated in transgenic rats expressing the human kallikrein-1 gene after myocardial infarction. - Rat Genome Database

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Cardiac function and remodeling is attenuated in transgenic rats expressing the human kallikrein-1 gene after myocardial infarction.

Authors: Koch, M  Spillmann, F  Dendorfer, A  Westermann, D  Altmann, C  Sahabi, M  Linthout, SV  Bader, M  Walther, T  Schultheiss, HP  Tschope, C 
Citation: Koch M, etal., Eur J Pharmacol. 2006 Nov 21;550(1-3):143-8. Epub 2006 Sep 7.
RGD ID: 1641799
Pubmed: PMID:17022964   (View Abstract at PubMed)
DOI: DOI:10.1016/j.ejphar.2006.08.054   (Journal Full-text)

Bradykinin coronary outflow, left ventricular performance and left ventricular dimensions of transgenic rats harboring the human tissue kallikrein-1 gene TGR(hKLK1) were investigated under basal and ischemic conditions. Bradykinin content in the coronary outflow of buffer-perfused, isolated hearts of controls and TGR(hKLK1) was measured by specific radioimmunoassay before and after global ischemia. Left ventricular function and left ventricular dimensions were determined in vivo using a tip catheter and echocardiography 6 days and 3 weeks after induction of myocardial infarction. Left ventricular type I collagen mRNA expression was analyzed by RNase protection assay. Compared to controls, basal bradykinin outflow was 3.5 fold increased in TGR(hKLK1). Ischemia induced an increase of bradykinin coronary outflow in controls but did not induce a further increase in TGR(hKLK1). However, despite similar unchanged infarction sizes, left ventricular function and remodeling improved in TGR(hKLK1) after myocardial infarction, indicated by an increase in left ventricular pressure (+34%; P<0.05), contractility (dp/dt max. +25%; P<0.05), and in ejection fraction (+20%; P<0.05) as well as by a reduction in left ventricular enddiastolic pressure (-49%, P<0.05), left ventricular enddiastolic diameter (-20%, P<0.05), and collagen mRNA expression (-15%, P<0.05) compared to controls. A chronically activated transgenic kallikrein kinin system with expression of human kallikrein-1 gene counteracts the progression of left ventricular contractile dysfunction after experimental myocardial infarction. Further studies have to show whether these results can be caused by other therapeutically options. Long acting bradykinin receptor agonists might be an alternative option to improve ischemic heart disease.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
KLK1Humanmyocardial infarction  IAGP  RGD 
Klk1c12Ratmyocardial infarction  ISOKLK1 (Homo sapiens) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Klk1c12  (kallikrein 1-related peptidase C12)

Genes (Homo sapiens)
KLK1  (kallikrein 1)


Additional Information