Abstract
Endothelin-1 (ET-1) modulates several vascular functions and plays an important role in the pathogenesis of insulin resistance. However, its role in the pathogenesis of impaired angiogenesis observed under insulin resistance conditions is not known. In the present study, we addressed this issue by analyzing the effect of ET-1 in human umbilical vein endothelial cells (HUVEC) on i) insulin-induced phosphorylation of two protein kinases involved in angiogenesis, Akt and ERK1/2, and on ii) insulin-induced angiogenesis in two in vitro models, those of Matrigel and of fibroblast/endothelial co-culture. Both insulin (100 ng/ml) and ET-1 (10 nmol/1) dose-dependently increased the phosphorylation of Akt and ERK1/2. Pre-treatment with ET-1 did not suppress the insulin-induced Akt and ERK1/2 phosphorylation. In the two in vitro models of angiogenesis, ET-1 did not inhibit insulin-induced angiogenesis. From these data we conclude that in vitro, at the times and at the concentrations examined, ET-1 does not impair insulin-induced angiogenesis.
| Original language | English |
|---|---|
| Pages (from-to) | 443-448 |
| Number of pages | 6 |
| Journal | International Journal of Molecular Medicine |
| Volume | 28 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Sep 2011 |
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Keywords
- Angiogenesis
- Endothelin
- Insulin
- Insulin-resistance
- Protein kinase
ASJC Scopus subject areas
- Genetics
Cite this
Endothelin-1 does not impair insulin-induced angiogenesis in vitro. / Pellegatta, Fabio; Brambilla, Claudia; Reduzzi, Alice; Bragheri, Marta; Zerbini, Gianpaolo; Catapano, Alberico L.
In: International Journal of Molecular Medicine, Vol. 28, No. 3, 09.2011, p. 443-448.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endothelin-1 does not impair insulin-induced angiogenesis in vitro
AU - Pellegatta, Fabio
AU - Brambilla, Claudia
AU - Reduzzi, Alice
AU - Bragheri, Marta
AU - Zerbini, Gianpaolo
AU - Catapano, Alberico L.
PY - 2011/9
Y1 - 2011/9
N2 - Endothelin-1 (ET-1) modulates several vascular functions and plays an important role in the pathogenesis of insulin resistance. However, its role in the pathogenesis of impaired angiogenesis observed under insulin resistance conditions is not known. In the present study, we addressed this issue by analyzing the effect of ET-1 in human umbilical vein endothelial cells (HUVEC) on i) insulin-induced phosphorylation of two protein kinases involved in angiogenesis, Akt and ERK1/2, and on ii) insulin-induced angiogenesis in two in vitro models, those of Matrigel and of fibroblast/endothelial co-culture. Both insulin (100 ng/ml) and ET-1 (10 nmol/1) dose-dependently increased the phosphorylation of Akt and ERK1/2. Pre-treatment with ET-1 did not suppress the insulin-induced Akt and ERK1/2 phosphorylation. In the two in vitro models of angiogenesis, ET-1 did not inhibit insulin-induced angiogenesis. From these data we conclude that in vitro, at the times and at the concentrations examined, ET-1 does not impair insulin-induced angiogenesis.
AB - Endothelin-1 (ET-1) modulates several vascular functions and plays an important role in the pathogenesis of insulin resistance. However, its role in the pathogenesis of impaired angiogenesis observed under insulin resistance conditions is not known. In the present study, we addressed this issue by analyzing the effect of ET-1 in human umbilical vein endothelial cells (HUVEC) on i) insulin-induced phosphorylation of two protein kinases involved in angiogenesis, Akt and ERK1/2, and on ii) insulin-induced angiogenesis in two in vitro models, those of Matrigel and of fibroblast/endothelial co-culture. Both insulin (100 ng/ml) and ET-1 (10 nmol/1) dose-dependently increased the phosphorylation of Akt and ERK1/2. Pre-treatment with ET-1 did not suppress the insulin-induced Akt and ERK1/2 phosphorylation. In the two in vitro models of angiogenesis, ET-1 did not inhibit insulin-induced angiogenesis. From these data we conclude that in vitro, at the times and at the concentrations examined, ET-1 does not impair insulin-induced angiogenesis.
KW - Angiogenesis
KW - Endothelin
KW - Insulin
KW - Insulin-resistance
KW - Protein kinase
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UR - http://www.scopus.com/inward/citedby.url?scp=79960020579&partnerID=8YFLogxK
U2 - 10.3892/ijmm.2011.689
DO - 10.3892/ijmm.2011.689
M3 - Article
C2 - 21537834
AN - SCOPUS:79960020579
VL - 28
SP - 443
EP - 448
JO - International Journal of Molecular Medicine
JF - International Journal of Molecular Medicine
SN - 1107-3756
IS - 3
ER -