Transcript Powerpoint
Microsomal Prostaglandin E2 Synthase-1 Deletion Leads to
Adverse Left Ventricular Remodeling After Myocardial
Infarction
by Norbert Degousee, Shafie Fazel, Denis Angoulvant, Eva Stefanski, SvenChristian Pawelzik, Marina Korotkova, Sara Arab, Peter Liu, Thomas F. Lindsay, Sun
Zhuo, Jagdish Butany, Ren-Ke Li, Laurent Audoly, Ronald Schmidt, Carlo Angioni,
Gerd Geisslinger, Per-Johan Jakobsson, and Barry B. Rubin
Circulation
Volume 117(13):1701-1710
April 1, 2008
Copyright © American Heart Association, Inc. All rights reserved.
Figure 1. Lack of mPGES-1 leads to LV dilation and impaired LV systolic and diastolic function
after MI. A, Survival after MI in Ptges+/+ (n=40) and Ptges−/− (n=40) mice.
Norbert Degousee et al. Circulation. 2008;117:1701-1710
Copyright © American Heart Association, Inc. All rights reserved.
Figure 2. Eccentric cardiomyocyte hypertrophy and altered expression of fetal cardiac genes in
mice lacking mPGES-1 after MI. A, Cardiomyocytes remote from the zone of infarction.
Norbert Degousee et al. Circulation. 2008;117:1701-1710
Copyright © American Heart Association, Inc. All rights reserved.
Figure 3. Differential activation of signaling cascades that regulate cardiomyocyte hypertrophy
in Ptges+/+ and Ptges−/− mice after MI. Western blot analysis of phospho-JNK2 (A), total JNK2
(B), phospho-ERK1 and phospho-ERK2 (C), total ERK1 and total ERK2 (D), phospho–GSK-α (E),
total GSK-α (F), phospho–PKC-δ (G), and calcineurin (H).
Norbert Degousee et al. Circulation. 2008;117:1701-1710
Copyright © American Heart Association, Inc. All rights reserved.
Figure 4. Attenuated PGE2 biosynthesis in the infarct and LV in Ptges−/− mice after MI. COX-2
(A) and mPGES-1 (B) mRNA levels in the LV after MI. COX-2 (C) and mPGES-1 mRNA (D) levels in
the infarct after MI. The infarct includes tissue from the infarction and adjacent peri-infarct
zones. mRNA was measured by quantitative real-time PCR, and results are normalized to
GAPDH mRNA levels.
Norbert Degousee et al. Circulation. 2008;117:1701-1710
Copyright © American Heart Association, Inc. All rights reserved.