[Promoting effects and mechanisms of prostaglandin E1 on proliferation and migration of endothelial cells].
Zhonghua Yi Xue Za Zhi
; 93(3): 222-5, 2013 Jan 15.
Article
en Zh
| MEDLINE
| ID: mdl-23570600
ABSTRACT
OBJECTIVE:
To investigate the mechanism(s) that prostaglandin E1 (PGE1) promotes human umbilical vein endothelial cell (HUVEC)proliferation and migration.METHODS:
Western blot, enzyme linked immunosorbent assay, cell proliferation and cell migration tests, and tube formation were used for analyzing the roles and mechanisms of PGE1 on HUVEC; Western blot was used for analyzing the effects of PGE1 on the expression of vascular endothelial growth factor (VEGF) in rat aortic vascular smooth muscle cells (VSMC).RESULTS:
PGE1 significantly increased VEGF expression of HUVEC in time and a dose dependent manner with concomitantly increased HUVEC proliferation; treatment of HUVEC with Bevacizumab apparently suppressed PGE1-stimulated VEGF expression, which led to decreased tube formation, reduced cell proliferation and migration by 41% and 38%, respectively, compared with PGE1 treatment alone; PGE1 time-dependently induced both phosphorylation of ERK and p38 in HUVEC, whereas ERK inhibitor, PD98059, or p38 inhibitor, SB203580, blocked PGE1-induced VEGF expression of HUVEC, resulting in dramatically suppression of HUVEC proliferation and migration compared with PGE1 treatment alone (60% and 55% by PD98059, 62% and 51% by SB203580, respectively); in addition, cAMP-dependent protein kinase A inhibitor, H89 or Rp-cAMP blocked PGE1-induced VEGF expression in VSMC.CONCLUSION:
PGE1 promotion of proliferation, migration and tube formation of HUVEC via VEGF further provides a novel theoretical support in efficacy of PGE1 treatment of critical limb ischemia and other related diseases.
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Bases de datos:
MEDLINE
Asunto principal:
Alprostadil
/
Miocitos del Músculo Liso
/
Células Endoteliales
/
Células Endoteliales de la Vena Umbilical Humana
/
Músculo Liso Vascular
Límite:
Animals
/
Humans
Idioma:
Zh
Revista:
Zhonghua Yi Xue Za Zhi
Año:
2013
Tipo del documento:
Article
País de afiliación:
China