Secretory expression of PR39 following adeno-associated viral-encoding fusion gene transfer induces angiogenesis in hypoxia chick embryo / 中华心血管病杂志
Chinese Journal of Cardiology
; (12): 746-749, 2009.
Article
en Zh
| WPRIM
| ID: wpr-236413
Biblioteca responsable:
WPRO
ABSTRACT
<p><b>OBJECTIVES</b>To investigate the impact of AAV-encoding NT4-TAT-His-PR39 fusion gene expression on HIF-1alpha level in ECV304 cultured under hypoxic condition (1%O(2)) and on angiogenesis in hypoxic chick embryo.</p><p><b>METHODS</b>PR39 cDNA was connected with NT4, TAT, 6 x His cDNA by molecular biology methods. The recombinant AAV vector was obtained by three plasmid co-transfection in 293 cells. Then ECV304 were respectively infected with AAV-NT4-TAT-His-PR39, 6 x His expression and HIF-1alpha level in ECV304 were detected by immunocytochemistry. The chicken embryos were randomized into the AAV-PR39, EV and PBS groups (n = 10 each) subject to hypoxia (5%O(2), n = 15) or normoxia environments (n = 15), the vessel density of the chicken chorioallantoic membrane (CAM) were measured by Image Pro Plus (IPP) software.</p><p><b>RESULTS</b>The expression of 6 x His protein was detected in AAV-PR39 infected ECV304 cells. HIF-1alpha protein activity was significantly increased in AAV-PR39 infected ECV304 underwent hypoxia compared to PBS and non-infected ECV304 groups (P < 0.05). The vessel density of chicken CAM in hypoxia environment but not in normoxia environment was also significantly higher in AAV-PR39 group than in EV group and PBS group (all P < 0.05).</p><p><b>CONCLUSION</b>AAV-encoding NT4-TAT-His-PR39 fusion gene expression significantly increased HIF-1alpha level in ECV304 exposed to hypoxia and promoted angiogenesis in hypoxic chicken embryo.</p>
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Índice:
WPRIM
Asunto principal:
Línea Celular
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Técnicas de Transferencia de Gen
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Dependovirus
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Neovascularización Fisiológica
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Péptidos Catiónicos Antimicrobianos
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Fusión Génica
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Genes Virales
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Genética
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Hipoxia
Límite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Cardiology
Año:
2009
Tipo del documento:
Article