Short-term delivery of anti-PlGF antibody delays progression of atherosclerotic plaques to vulnerable lesions
Aims: placental growth factor (PlGF), a homologue of vascular endothelial growth factor, is a pleiotropic cytokine with a pro-inflammatory activity. Previous gene-inactivation studies revealed that the loss of PlGF delays atherosclerotic lesion development and inhibits macrophage infiltration, but t...
| Autores: | , , , , , , , , , , , |
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| Tipo de recurso: | artículo |
| Estado: | Versión aceptada para publicación |
| Fecha de publicación: | 2009 |
| País: | España |
| Institución: | Universidad Pública de Navarra |
| Repositorio: | Academica-e. Repositorio Institucional de la Universidad Pública de Navarra |
| OAI Identifier: | oai:academica-e.unavarra.es:2454/56169 |
| Acceso en línea: | https://hdl.handle.net/2454/56169 |
| Access Level: | acceso abierto |
| Palabra clave: | PlGF Atherosclerosis Inflammation PlGF neutralization |
| Sumario: | Aims: placental growth factor (PlGF), a homologue of vascular endothelial growth factor, is a pleiotropic cytokine with a pro-inflammatory activity. Previous gene-inactivation studies revealed that the loss of PlGF delays atherosclerotic lesion development and inhibits macrophage infiltration, but the activity of an anti-PlGF antibody (αPlGF mAb) has not been evaluated yet. Methods and results: we characterized the potential of short-term delivery of αPlGF mAb in inhibiting lesion development in ApoE-deficient mice (apoE−/−) and in CD4:TGFβRIIDN x apoE−/− mice, a more severe atherosclerosis model. Short-term treatment of αPlGF mAb reduces early atherosclerotic plaque size and inflammatory cell infiltration in the lesion. Conclusion: these pharmacological αPlGF mAb results confirm previous genetic evidence that inhibition of PlGF slows down early atherosclerotic lesion development. Furthermore, the phenocopy of genetic and pharmacological loss-of-function strategies underscores that αPlGF acts by selectively neutralizing PlGF. |
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