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EnglishThrombopoietin (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 (PSer1179) 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; 10 nM) 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.
| Titolo: | A novel role of thrombopoietin as a physiological modulator of coronary flow | |
| Autori Riconosciuti: | ||
| Autori: | Roberta Ramella; Maria Pia Gallo; Tiziana Spatola; Enrico Lupia; Giuseppe Alloatti | |
| Data di pubblicazione: | 2011 | |
| Abstract: | 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 (PSer1179) 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; 10 nM) 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. | |
| Volume: | 167 | |
| Pagina iniziale: | 5 | |
| Pagina finale: | 8 | |
| Digital Object Identifier (DOI): | 10.1016/j.regpep.2010.12.008 | |
| Parole Chiave: | Thrombopoietin; Coronary flow; Endothelium; Nitric Oxide | |
| Rivista: | REGULATORY PEPTIDES | |
| Appare nelle tipologie: | 03A-Articolo su Rivista |
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