Regul Pept 2011,
PMID: 21237210
Ramella, Roberta; Gallo, Maria Pia; Spatola, Tiziana; Lupia, Enrico; Alloatti, Giuseppe
Thrombopoietin (TPO) is known for its ability to stimulate platelet production. However, little is currently known whether TPO plays a physiological function in the heart. The potential vasodilatory role of TPO was tested on the isolated rat heart. The expression of TPO receptor (c-mpl) and the TPO-dependent eNOS phosphorylation (P(Ser1179)) were studied on Cardiac-derived normal Human Micro Vascular Endothelial Cells (HMVEC-C) by Western blot analysis. While TPO (10-200 pg/mL) did not modify coronary flow (CF) under basal conditions, it reduced the coronary constriction caused by endothelin-1 (ET-1; 10nM) in a dose-dependent manner. This effect was blocked by both Wortmannin (100 nM) and L-NAME (100 nM); on HMVEC-C, TPO induced eNOS phosphorylation through a Wortmannin sensitive mechanism. Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce PI3K/Akt-dependent eNOS phosphorylation and NO release.
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Text Mining Data
eNOS → TPO: "
The expression of TPO receptor ( c-mpl ) and the
TPO dependent
eNOS phosphorylation ( P ( Ser1179 ) ) were studied on Cardiac derived normal Human Micro Vascular Endothelial Cells ( HMVEC-C ) by Western blot analysis
"
TPO → eNOS: "
This effect was blocked by both Wortmannin ( 100 nM ) and L-NAME ( 100 nM ) ; on HMVEC-C, TPO induced eNOS phosphorylation through a Wortmannin sensitive mechanism
"
TPO → eNOS: "
Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce PI3K/Akt dependent eNOS phosphorylation and NO release
"
eNOS → PI3K/Akt: "
Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce PI3K/Akt dependent eNOS phosphorylation and NO release
"
eNOS → PI3K/Akt: "
Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce PI3K/Akt dependent eNOS phosphorylation and NO release
"
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