Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice

Journal of Clinical Investigation

Volumn 117, Issue 11, 2007, Pages 3188-3197

  Tirziu, Daniela ^a   Chorianopoulos, Emmanuel ^b   Moodie, Karen L ^a   Palac, Robert T ^a   Zhuang, Zhen W ^a   Tjwa, Marc ^b   Roncal, Carmen ^b   Eriksson, Ulf ^c   Fu, Qiangwei ^a   Elfenbein, Arye ^a   Hall, Amy E ^a   Carmeliet, Peter ^b   Moons, Lieve ^b   Simons, Michael ^a,d  

^a DARTMOUTH MEDICAL SCHOOL   (United States)

^b UNIVERSITY OF LEUVEN   (Belgium)

^c LUDWIG INSTITUTE FOR CANCER RESEARCH   (Sweden)

^d DARTMOUTH HITCHCOCK MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANGIOGENIC FACTOR; ENDOTHELIAL NITRIC OXIDE SYNTHASE; MITOGEN ACTIVATED PROTEIN KINASE; N(G) NITROARGININE METHYL ESTER; NATRIURETIC FACTOR; NITRIC OXIDE SYNTHASE INHIBITOR; PROTEIN; PROTEIN KINASE B; PROTEIN PR39; TRANSCRIPTION FACTOR GATA 4; UNCLASSIFIED DRUG; VASCULOTROPIN B;

ANGIOGENESIS; ANIMAL CELL; ANIMAL EXPERIMENT; ARTICLE; CONTROLLED STUDY; HEART BLOOD VESSEL; HEART SIZE; HEART VENTRICLE HYPERTROPHY; HEART WEIGHT; MOUSE; NEWBORN; NONHUMAN; NUCLEOTIDE SEQUENCE; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; TRANSGENIC MOUSE;

ANGIOGENIC PROTEINS; ANIMALS; CARDIOMEGALY; CELLS, CULTURED; ECHOCARDIOGRAPHY; ENDOTHELIAL CELLS; ENZYME INHIBITORS; HEART; HEMODYNAMICS; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; MYOCARDIUM; MYOCYTES, CARDIAC; NEOVASCULARIZATION, PHYSIOLOGIC; NG-NITROARGININE METHYL ESTER; ORGAN SIZE; RATS; RATS, SPRAGUE-DAWLEY; TRANSGENES;

EID: 36048999385     PISSN: 00219738     EISSN: 15588238     Source Type: Journal    
DOI: 10.1172/JCI32024     Document Type: Article

References (26)

1. Dallabrida, S.M., et al. 2003. Adipose tissue growth and regression are regulated by angiopoietin-1. Biochem. Biophys. Res. Commun. 311:563-571.
2. Folkman, J. 1998. Is tissue mass regulated by vascular endothelial cells? Prostate as the first evidence. Endocrinology. 139:441-442.
3. Greene, A.K., et al. 2003. Endothelial-directed hepatic regeneration after partial hepatectomy. Ann. Surg. 237:530-535.
4. Hunter, J.J., and Chien, K.R. 1999. Signaling pathways for cardiac hypertrophy and failure. N. Engl. J. Med. 341:1276-1283.
5. Lorell, B.H., and Carabello, B.A. 2000. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. Circulation. 102:470-479.
6. Gavin, J.B., Maxwell, L., and Edgar, S.G. 1998. Microvascular involvement in cardiac pathology. J. Mol. Cell. Cardiol. 30:2531-2540.
7. Shiojima, I., et al. 2005. Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. J. Clin. Invest. 115:2108-2118. doi:10.1172/JCI24682.
8. Suzuki, G., Lee, T.C., Fallavollita, J.A., and Canty, J.M., Jr. 2005. Adenoviral gene transfer of FGF-5 to hibernating myocardium improves function and stimulates myocytes to hypertrophy and reenter the cell cycle. Circ. Res. 96:767-775.
9. Li, J., et al. 2000. PR39, a peptide regulator of angiogenesis. Nat. Med. 6:49-55.
10. Hu, R.G., et al. 2005. The N-end rule pathway as a nitric oxide sensor controlling the levels of multiple regulators. Nature. 437:981-986.
11. Bao, J., et al. 2001. PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated I kappa B alpha degradation. Am. J. Physiol. Heart Circ. Physiol. 281:H2612-H2618.
12. Bellomo, D., et al. 2000. Mice lacking the vascular endothelial growth factor-B gene (Vegfb) have smaller hearts, dysfunctional coronary vasculature, and impaired recovery from cardiac ischemia. Circ. Res. 86:E29-E35.
13. Tomanek, R.J., and Busch, T.L. 1998. Coordinated capillary and myocardial growth in response to thyroxine treatment. Anat. Rec. 251:44-49.
14. Dor, Y., et al. 2002. Conditional switching of VEGF provides new insights into adult neovascularization and pro-angiogenic therapy. EMBO J. 21:1939-1947.
15. Drab, M., et al. 2001. Loss of caveolae, vascular dysfunction, and pulmonary defects in caveolin-1 gene-disrupted mice. Science. 293:2449-2452.
16. Razani, B., et al. 2001. Caveolin-1 null mice are viable but show evidence of hyperproliferative and vascular abnormalities. J. Biol. Chem. 276:38121-38138.
17. Woodman, S.E., et al. 2002. Caveolin-3 knock-out mice develop a progressive cardiomyopathy and show hyperactivation of the p42/44 MAPK cascade. J. Biol. Chem. 277:38988-38997.
18. Brunner, F., Andrew, P., Wolkart, G., Zechner, R., and Mayer, B. 2001. Myocardial contractile function and heart rate in mice with myocyte-specific overexpression of endothelial nitric oxide synthase. Circulation. 104:3097-3102.
19. Brunner, F., et al. 2003. Attenuation of myocardial ischemia/reperfusion injury in mice with myocytespecific overexpression of endothelial nitric oxide synthase. Cardiovasc. Res. 57:55-62.
20. Izumiya, Y., et al. 2006. Vascular endothelial growth factor blockade promotes the transition from compensatory cardiac hypertrophy to failure in response to pressure overload. Hypertension. 47:887-893.
21. Shiojima, I., and Walsh, K. 2006. Regulation of cardiac growth and coronary angiogenesis by the Akt/ PKB signaling pathway. Genes Dev. 20:3347-3365.
22. Sano, M., et al. 2007. p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload. Nature. 446:444-448.
23. Yu, Z., Redfern, C.S., and Fishman, G.I. 1996. Conditional transgene expression in the heart. Circ. Res. 79:691-697.
24. Eppihimer, M.J., et al. 1998. Differential expression of platelet-endothelial cell adhesion molecule-1 (PECAM-1) in murine tissues. Microcirculation. 5:179-188.
25. Heymans, S., et al. 1999. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat. Med. 5:1135-1142.
26. Luttun, A., et al. 2002. Revascularization of ischemic tissues by PlGF treatment, and inhibition of tumor angiogenesis, arthritis and atherosclerosis by anti-Flt1. Nat. Med. 8:831-840.