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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: Dev Dyn. 2011 Feb;240(2):384–393. doi: 10.1002/dvdy.22549

Fig. 5.

Fig. 5

Endothelial-specific deletion of Cxcr7 causes cardiac semilunar valve stenosis and secondary hypertrophy. A: Image of whole hearts taken from 6-month-old wild-type or Tie2-Cre;Cxcr7flox/− mice. Endothelial-specific deletion of Cxcr7 caused marked hypertrophy. B: Transverse sections of wild-type and Tie2-Cre;Cxcr7flox/− mice. The mutant heart has a thicker ventricular wall than the wild-type heart but a similarly sized ventricular cavity. C: Left ventricular posterior wall (LVPW) thickness, measured by echocardiography, was ∼1.4-fold thicker in Tie2-Cre;Cxcr7flox/− hearts than in wild-type hearts (n=3 per group, *P<0.05). Heart sections of 6-month-old wild-type or Tie2-Cre;Cxcr7flox/− mice were stained with hematoxylin-eosin. Tie2-Cre;Cxcr7flox/− mice had aortic valve (AoV) stenosis similar to that in Cxcr7−/− mice but a milder pulmonary valve (PV) phenotype. H,I: Magnified images (20×) of wild-type and Tie2-Cre;Cxcr7flox/− heart sections stained with hematoxylin-eosin. Myocardial structure was disarrayed and the myocytes were not well-packed in mutant hearts. J,K: Masson's trichrome staining showed more collagen deposition (blue) in Tie2-Cre;Cxcr7flox/− hearts than in wild-type hearts.