n addition to its central role in blood coagulation and hemostasis, human α-thrombin is a growth factor for a variety of cell types, including monocytes and endothelial cells, involved in the control of angiogenesis. Different cytokines produced by mononuclear cells have been implicated in angiogenic processes associated with tissue repair and certain human malignancies. We have previously shown that thrombin enhances proliferative responses in T lymphocytes. More recently, we reported that interferon-γ-differentiated monocytes have increased expression of protease-activatedreceptor-1 (PAR-1) and increased thrombin binding. Since cytokines may be involved directly and indirectly in angiogenesis, we initiated studies to determine thrombin effects on the induction of cytokines, such as interleukin (IL)-1 and IL-6, in human mononuclear cells. IL-1 and IL-6 protein expression was significantly enhanced by thrombin (P<.05), as determined by enzyme-linked immunosorbent assay (ELISA). Treating mononuclear cells with the PAR-1 peptide, SFLLRN, has effects similar to those of thrombin. Thus, it appears that these thrombin effects are mediated through activation of PAR-1. These results confirm that thrombin is a strong activator of monocytes and could be involved in angiogenesis by inducing cytokines that could enhance the angiogenic process in tissue repair.

Naldini, A., Carney, D.H., Pucci, A., Pasquali, A., Carraro, F. (2002). Thrombin regulates the expression of pro-angiogenic cytokines via proteolytic activation of protease-activated receptor-1. GENERAL PHARMACOLOGY, 35(5), 255-259 [10.1016/S0306-3623(01)00113-6].

Thrombin regulates the expression of pro-angiogenic cytokines via proteolytic activation of protease-activated receptor-1

NALDINI, A.;PUCCI, A.;CARRARO, F.
2002-01-01

Abstract

n addition to its central role in blood coagulation and hemostasis, human α-thrombin is a growth factor for a variety of cell types, including monocytes and endothelial cells, involved in the control of angiogenesis. Different cytokines produced by mononuclear cells have been implicated in angiogenic processes associated with tissue repair and certain human malignancies. We have previously shown that thrombin enhances proliferative responses in T lymphocytes. More recently, we reported that interferon-γ-differentiated monocytes have increased expression of protease-activatedreceptor-1 (PAR-1) and increased thrombin binding. Since cytokines may be involved directly and indirectly in angiogenesis, we initiated studies to determine thrombin effects on the induction of cytokines, such as interleukin (IL)-1 and IL-6, in human mononuclear cells. IL-1 and IL-6 protein expression was significantly enhanced by thrombin (P<.05), as determined by enzyme-linked immunosorbent assay (ELISA). Treating mononuclear cells with the PAR-1 peptide, SFLLRN, has effects similar to those of thrombin. Thus, it appears that these thrombin effects are mediated through activation of PAR-1. These results confirm that thrombin is a strong activator of monocytes and could be involved in angiogenesis by inducing cytokines that could enhance the angiogenic process in tissue repair.
Naldini, A., Carney, D.H., Pucci, A., Pasquali, A., Carraro, F. (2002). Thrombin regulates the expression of pro-angiogenic cytokines via proteolytic activation of protease-activated receptor-1. GENERAL PHARMACOLOGY, 35(5), 255-259 [10.1016/S0306-3623(01)00113-6].
File in questo prodotto:
File Dimensione Formato  
Thrombin regulates the expression of proangiogenic cytokines via proteolytic activation protease activated receptor 1 (Gen Pharmacol2002).pdf

non disponibili

Tipologia: Abstract
Licenza: NON PUBBLICO - Accesso privato/ristretto
Dimensione 1.05 MB
Formato Adobe PDF
1.05 MB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/38708
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo