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Activation of the cardiac renin-angiotensin system and increased myocardial collagen expression in human aortic valve disease

Jens Fielitz, MD^*, Stefan Hein, MD, Veselin Mitrovic, MD, Rainer Pregla, MD, Heinz R. Zurbrügg, MD, Christina Warnecke, VMD^*, Jutta Schaper, MD, Eckart Fleck, MD^* and Vera Regitz-Zagrosek, MD^*

^* Innere Medizin, Kardiologie, Charite, Campus Virchow Klinikum, Humboldt Universität Berlin und Deutsches Herzzentrum, Berlin, Germany
Kerkhoff-Klinik, Abt für Herz-, Gefäß- und Thoraxchirurgie, Bad Nauheim, Germany
Klinik für Herz-, Gefäß- und Thoraxchirurgie, DHZB?2, Germany
MPI für experimentelle Kardiologie, Bad Nauheim, Germany

View larger version (31K): [in a new window]   Figure 1 Expression of ACE, TGF-beta1 and collagen I mRNA in patients with AS and AR. Bar graphs show ACE/GAPDH (left); TGF-beta1/PDH (middle); and collagen (Col) I/GAPDH (right) expression in control hearts (Con), patients with AS and patients with AR. The expression of ACE mRNA and TGF-beta1 mRNA was significantly increased in AR and AS. The collagen I mRNA was significantly increased in AS and was elevated in AR, without reaching the level of statistical significance. The mean values ± SEM are presented, and analysis of variance was performed, with the Bonferroni-corrected (Tamhane-T2 procedure) p values indicated. n.s. = not significant.

View larger version (30K): [in a new window]   Figure 2 Expression of ACE, hHC, TGF-beta1, collagen I and III and fibronectin mRNA in patients with AS and normal or impaired LVEF. The bar graph shows ACE/GAPDH; chymase/GAPDH; TGF-beta1/PDH; collagen (Col) I/GAPDH; collagen III/GAPDH; and fibronectin (Fn)/GAPDH expression in patients with AS and normal or impaired LVEF (>55%, <55%, respectively). The ACE mRNA, hHC, TGF-beta1 and collagen I mRNA expression was significantly altered in both groups, whereas the increase in collagen III and fibronectin mRNA only reached statistical significance in patients with AS and impaired LVEF. The mean values ± SEM are presented, and analysis of variance was performed, with the Bonferroni-corrected (Tamhane-T2 procedure) p values indicated. n.s. = not significant. *p < 0.05. **p < 0.01.

View larger version (98K): [in a new window]   Figure 3 Immunofluorescence for collagen, fibronectin, ACE and TGF-beta1. Row I (top) = immunofluorescence for collagen I (green, nuclei are red). (A) Normal myocardium with fine septa surrounding the myocytes and capillaries. (B) In hypertrophied myocardium, the amount of collagen I between the myocytes is increased. Row II = immunofluorescence for TGF-beta1 (green, myocytes are red by phalloidin). (A) In normal myocardium, only a few cells in the interstitium are positive for TGF-beta1. (B) In hypertrophied myocardium, numerous structures contain TGF-beta1 as fine granules. Row III = immunofluorescence for fibronectin (green, nuclei are red). (A) Normal myocardium shows fine layers of fibronectin between the myocytes, corresponding to labeling for collagen I. (B) In hypertrophied myocardium, the amount of fibronectin is greatly increased. In three-dimensional reconstruction in the confocal microscope, the myocytes are blue. Row IV (bottom) = immunofluorescence for ACE (green, nuclei are red). (A) Only a few small capillaries are positive for ACE in normal myocardium. (B) In hypertrophied myocardium, labeling for ACE is more prominent.