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La exposición a los andrógenos aumenta la adhesión de los monocitos humanos al endotelio vascular y la expresión de
J A McCrohon1, W Jessup, D J Handelsman
1Heart Research Institute, Departments of Cardiology and Andrology, Royal Prince Alfred Hospital, Sydney, Australia. janem@card.rpa.cs.nsw.gov.au
Circulation
|May 5, 1999
Resumen
Los andrógenos como la dihidrotestosterona (DHT) aumentan la adhesión de los monocitos a las células endoteliales, un paso clave en la aterosclerosis. Este efecto está mediado por la molécula de adhesión celular vascular-1 (VCAM-1) y puede ser bloqueado por los bloqueadores de los receptores de andrógenos.
Área de la Ciencia:
- Endocrinología Endocrinología.
- Biología Cardiovascular Biología Cardiovascular
- Inmunología Inmunología.
Sus antecedentes:
- El sexo masculino es un factor de riesgo conocido para la enfermedad de las arterias coronarias (CAD).
- La adhesión de los monocitos a las células endoteliales es crítica en el desarrollo de la aterosclerosis.
- Los andrógenos pueden desempeñar un papel en la promoción de este proceso de adhesión.
Objetivo del estudio:
- Para investigar el efecto de la dihidrotestosterona (DHT) en la adhesión de los monocitos a las células endoteliales.
- Para examinar el impacto de la DHT en las moléculas de adherencia de la superficie celular endotelial.
- Para determinar si el bloqueo del receptor de andrógenos afecta la adhesión monocítica inducida por DHT.
Principales métodos:
- Las células endoteliales de la vena umbilical humana (HUVEC) fueron tratadas con DHT y/o hidroxiflutamida (HF).
- La adhesión de los monocitos a las HUVEC se midió mediante microscopía de luz.
- La expresión de la molécula de adherencia de la superficie celular endotelial (VCAM-1) se cuantificó utilizando ELISA.
Principales resultados:
- La DHT aumentó significativamente la adhesión de los monocitos a las HUVEC de una manera dependiente de la dosis.
- La DHT elevó la expresión de la molécula de adhesión celular vascular-1 (VCAM-1) en las células endoteliales.
- La hidroxiflutamida (HF) bloqueó tanto el aumento de la adhesión como la expresión de VCAM-1, al igual que los anticuerpos anti-VCAM-1.
Conclusiones:
- La exposición a los andrógenos promueve la adhesión de los monocitos a las células endoteliales.
- Este efecto proaterogénico está, en parte, mediado por el aumento de la expresión de VCAM-1.
- La orientación de las vías androgénicas o VCAM-1 puede ofrecer estrategias terapéuticas para la aterosclerosis.
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