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Effects of insulin like growth factor-1 on cell viability and tissue factor in vascular endothelial cells / 中华血液学杂志
Chinese Journal of Hematology ; (12): 605-608, 2007.
Article de Zh | WPRIM | ID: wpr-262975
Bibliothèque responsable: WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To study the effects of insulin like growth factor-1 (IGF-1) on cell viability and tissue factor (TF) in angiotensin II (Ang II) induced vascular endothelial cells and to investigate its mechanisms.</p><p><b>METHODS</b>10(-6) mol/L Ang II was added to human vascular endothelial cells (HUVECs) culture media alone or 30 min after pretreatment with IGF-1 (0.1 microg/ml , 0.5 microg/ml, 2.5 microg/ml). Cell viability and AngII type 1 receptor (AT1-R) mRNA were evaluated after 24 h incubation with AngII. At the optimum concentration of IGF-1 affecting cell viability, the time dependent manner for 12 - 48 h incubation with Ang II was evaluated. TF, NOS and NO were investigated after 24 h incubation with Ang II. In addition, NO synthase inhibitor Nomega-nitro-1-arginine methylester(L-NAME) was added 30 min before addition of IGF-1 and Ang II, and cell viability, TF, AT1-R mRNA, NOS and NO were evaluated after 24 h incubation.</p><p><b>RESULTS</b>(1) Ang II induced a decrease in cell vitality, an upregulation of AT1-R mRNA, an increase in TF, and a decrease in the activity of NOS and content of NO. (2) Pretreatment with IGF-1 significantly inhibited the decreased cell viability and upregulation of AT1-R mRNA. IGF-1 at 0.5 microg/ml showed the most obvious effects. This effect of cell viability recovery was in a time dependent manner during 12 -48 h. (3) IGF-1 also inhibited the increased content of TF, the decreased activity of NOS and the decreased content of NO. (4) The beneficial effects of IGF-1 on cultured endothelial cells were completely abolished by L-NAME.</p><p><b>CONCLUSION</b>IGF-1 pretreatment could enhance the ang II injured cell viability and anti-thrombosis capacity, and the protective effects may be related to activation of NOS-NO signaling pathway which inhibited AT1-R.</p>
Sujet(s)
Texte intégral: 1 Indice: WPRIM Sujet Principal: Pharmacologie / Physiologie / Thromboplastine / Facteur de croissance IGF-I / Angiotensine-II / Survie cellulaire / Cellules cultivées / Nitric oxide synthase / Cellules endothéliales / Récepteur de type 1 à l'angiotensine-II Limites du sujet: Humans langue: Zh Texte intégral: Chinese Journal of Hematology Année: 2007 Type: Article
Texte intégral: 1 Indice: WPRIM Sujet Principal: Pharmacologie / Physiologie / Thromboplastine / Facteur de croissance IGF-I / Angiotensine-II / Survie cellulaire / Cellules cultivées / Nitric oxide synthase / Cellules endothéliales / Récepteur de type 1 à l'angiotensine-II Limites du sujet: Humans langue: Zh Texte intégral: Chinese Journal of Hematology Année: 2007 Type: Article