Search

Growth hormone (GH) plays a physiological role in the immune system. In macrophages, GH enhances the production of hydrogen peroxide, superoxide anions, nitric oxide, cytokines, and chemokines, including interferon-γ and macrophage inflammatory protein-1α. However, some of the effects of GH stimulation on the biological functions of macrophages remain to be elucidated. Herein, we showed that in vivo GH treatment resulted in decreased expression of VLA-5 and VLA-6 integrins on the macrophage surface, accompanied by a reduction in macrophage adhesion to extracellular matrix (ECM) ligands, fibronectin, and laminin. Additionally, a decrease in macrophage adhesion to laminin was observed when the cells were treated in vitro with GH. In transwell migration assays, GH-treated macrophages showed increased migration after 6 h. Although in vitro GH treatment did not influence the phagocytic activity of macrophages, when the treatment was performed in vivo, peritoneal macrophages from GH-treated mice showed a higher percentage of phagocytosis and higher phagocytic capacity than cells from control animals. These results led us to analyse the role of insulin-like growth factor-1 (IGF-1), a GH stimulated factor, on macrophage phagocytosis. We observed an increase in phagocytic activity when J774 murine macrophages were treated with IGF-1 for 24 h. Our results revealed an important role for GH in resident macrophage migration and phagocytic activity. Specifically, we demonstrate that IGF-1 may be the GH stimulated factor that induces macrophage phagocytosis in vivo.

The generation of new blood vessels is a complex process mediated by a variety of growth factors, and the growth hormone (GH) has been shown to act as a proangiogenic factor. In fact, human GH deficiency or excess are associated with endothelial dysfunction. Moreover, mouse models have revealed the action of GH in both tissue repair and in the microvascular circulation of normal tissues. In this study, we investigated the in vitro effects of GH on endothelial cells. Using a murine endothelioma cell line (tEnd.1), we demonstrated that GH has a mitogenic effect. The hormone also affected the endothelial cellular morphology and augmented the deposition of the extracellular matrix molecules, laminin, and fibronectin, on tEnd.1 surface. GH could stimulate tEnd.1 cell fugetaxis, in transwell chambers migration assay, and increased the formation of capillary-like structures in Matrigel®-coated plates. Given the important role of angiogenesis during tissue injury, for example, at ischemic lesions, these findings shed light on therapeutic angiogenesis, particularly in pathologies where the cardiovascular system has been compromised.

Growth hormone (GH) plays a physiological role in the immune system. In macrophages, GH enhances the production of hydrogen peroxide, superoxide anions, nitric oxide, cytokines, and chemokines, including interferon-γ and macrophage inflammatory protein-1α. However, some of the effects of GH stimulation on the biological functions of macrophages remain to be elucidated. Herein, we showed that in vivo GH treatment resulted in decreased expression of VLA-5 and VLA-6 integrins on the macrophage surface, accompanied by a reduction in macrophage adhesion to extracellular matrix (ECM) ligands, fibronectin, and laminin. Additionally, a decrease in macrophage adhesion to laminin was observed when the cells were treated in vitro with GH. In transwell migration assays, GH-treated macrophages showed increased migration after 6 h. Although in vitro GH treatment did not influence the phagocytic activity of macrophages, when the treatment was performed in vivo, peritoneal macrophages from GH-treated mice showed a higher percentage of phagocytosis and higher phagocytic capacity than cells from control animals. These results led us to analyse the role of insulin-like growth factor-1 (IGF-1), a GH stimulated factor, on macrophage phagocytosis. We observed an increase in phagocytic activity when J774 murine macrophages were treated with IGF-1 for 24 h. Our results revealed an important role for GH in resident macrophage migration and phagocytic activity. Specifically, we demonstrate that IGF-1 may be the GH stimulated factor that induces macrophage phagocytosis in vivo.

The generation of new blood vessels is a complex process mediated by a variety of growth factors, and the growth hormone (GH) has been shown to act as a proangiogenic factor. In fact, human GH deficiency or excess are associated with endothelial dysfunction. Moreover, mouse models have revealed the action of GH in both tissue repair and in the microvascular circulation of normal tissues. In this study, we investigated the in vitro effects of GH on endothelial cells. Using a murine endothelioma cell line (tEnd.1), we demonstrated that GH has a mitogenic effect. The hormone also affected the endothelial cellular morphology and augmented the deposition of the extracellular matrix molecules, laminin, and fibronectin, on tEnd.1 surface. GH could stimulate tEnd.1 cell fugetaxis, in transwell chambers migration assay, and increased the formation of capillary-like structures in Matrigel®-coated plates. Given the important role of angiogenesis during tissue injury, for example, at ischemic lesions, these findings shed light on therapeutic angiogenesis, particularly in pathologies where the cardiovascular system has been compromised.