Lessons learned from cancer may help in the treatment of pulmonary hypertension

Journal of Clinical Investigation

Volumn 115, Issue 6, 2005, Pages 1461-1463

  Adnot, Serge ^a,b  

^a HENRI MONDOR HOSPITAL   (France)

^b FACULTÉ DE MÉDECINE   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOVIRUS VECTOR; ANTIHYPERTENSIVE AGENT; MONOCROTALINE; PROTEIN INHIBITOR; SURVIVIN;

APOPTOSIS; ARTERY MUSCLE; CANCER; HUMAN; HYPERPLASIA; PRIORITY JOURNAL; PROGNOSIS; PROTEIN EXPRESSION; PULMONARY HYPERTENSION; REVIEW;

EID: 20444501324     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI25399     Document Type: Review

References (18)

1. Deng, Z., et al. 2000. Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene. Am. J. Hum. Genet. 67:737-744.
2. Lane, K., et al. 2000. Heterozygous germline mutations in BMPR2, encoding a TGF-beta receptor, cause familial primary pulmonary hypertension. The International PPH Consortium. Nat. Genet. 26:3-4.
3. Eddahibi, S., Morrell, N., d'Ortho, M., Naeije, R., and Adnot, S. 2002. Pathobiology of pulmonary arterial hypertension. Eur. Respir. J. 20:1559-1572.
4. Eddahibi, S., et al. 2001. Serotonin transporter overexpression is responsible for pulmonary artery smooth muscle hyperplasia in primary pulmonary hypertension. J. Clin. Invest. 108:1141-1150. doi:10.1172/JCI200112805.
5. Marcos, E., et al. 2004. Serotonin-induced smooth muscle hyperplasia in various forms of human pulmonary hypertension. Circ. Res. 94:1263-1270.
6. Morrell, N.W., et al. 2001. Altered growth responses of pulmonary artery smooth muscle cells from patients with primary pulmonary hypertension to transforming growth factor-beta(1) and bone morphogenetic proteins. Circulation. 104:790-795.
7. Atkinson, C., et al. 2002. Primary pulmonary hypertension is associated with reduced pulmonary vascular expression of type II bone morphogenetic protein receptor. Circulation. 105:1672-1678.
8. Lee, S.D., et al. 1998. Monoclonal endothelial cell proliferation is present in primary but not secondary pulmonary hypertension. J. Clin. Invest. 101:927-934.
9. McMurtry, M.S., et al. 2005. Gene therapy targeting survivin selectively induces pulmonary vascular apoptosis and reverses pulmonary arterial hypertension. J. Clin. Invest. 115:1479-1491. doi:10.1172/JCI23203.
10. Salvesen, G.S., and Duckett, C.S. 2002. IAP proteins: blocking the road to death's door. Nat. Rev. Mol. Cell Biol. 3:401-410.
11. Altieri, D.C. 2003. Validating survivin as a cancer therapeutic target. Nat. Rev. Cancer. 3:46-54.
12. Blanc-Brude; O.P., et al. 2002. Inhibitor of apoptosis protein survivin regulates vascular injury. Nat. Med. 8:987-994.
13. Conway, E.M., et al. 2003. Survivin-dependent angiogenesis in ischemic brain: molecular mechanisms of hypoxia-induced up-regulation. Am. J. Pathol. 163:935-946.
14. Tran, J., et al. 2002. A role for survivin in chemoresistance of endothelial cells mediated by VEGF. Proc. Natl Acad. Sci. U. S. A. 99:4349-4354.
15. Kato, J., et al. 2001. Expression of survivin in esophageal cancer: correlation with the prognosis and response to chemotherapy. Int. J. Cancer. 95:92-95.
16. Monzo, M., et al. 1999. A novel anti-apoptosis gene: re-expression of survivin messenger RNA as a prognosis marker in non-small-cell lung cancers. J. Clin. Oncol. 17:2100-2104.
17. Mesri, M., Wall, N.R., Li, J., Kim, R.W., and Altieri, D.C. 2001. Cancer gene therapy using a survivin mutant adenovirus. J. Clin. Invest. 108:981-990. doi:10.1172/JCI200112983.
18. Wang, K., Brems, J., Gamelli, R., and Ding, J. 2005. Reversibility of caspase activation and its role during glycochenodeoxycholate-induced hepatocyte apoptosis. J. Biol. Chem. doi:10.1074/jbc.M411607200.