TY - JOUR
T1 - Wnt3a promotes pro-angiogenic features in macrophages in vitro
T2 - Implications for stroke pathology
AU - Fuster-Matanzo, Almudena
AU - Manferrari, Giulia
AU - Marchetti, Bianca
AU - Pluchino, Stefano
PY - 2017/1/1
Y1 - 2017/1/1
N2 - Wnt3a is implicated in several key cellular processes and its expression has been reported in different cell types. Here, we report a novel function for Wnt3a in macrophages, whose exposure to this ligand shifts them towards a pro-angiogenic phenotype capable, under oxygen and glucose deprivation, of inducing in vitro tubular pattern structures in endothelial cells resembling capillary-like vasculature. These newly acquired angiogenetic features also include increased proliferation and migration and surprisingly, an increase in cell death. This work provides a new link between Wnt3a and macrophage-mediated angiogenesis under glucose and oxygen deprivation in vitro, which are worth further investigation in pathological conditions including stroke, where the stimulation of the angiogenic process might help to recovery after tissue injury Impact statement This work provides a new link between Wnt3a and macrophage-mediated angiogenesis under glucose and oxygen deprivation in vitro. Our results reveal how Wnt3a shifts macrophages towards a pro-angiogenic phenotype, which is able-in absence of both glucose and oxygen-of inducing angiogenesis in vitro, thus pointing to a synergy between the activation of the pathway and the hypoxia scenario. This work also demonstrates that modulation of cell death is key in order to explain the observed angiogenic effects. We consider all these findings of significant importance, since no connection between Wnt3a, macrophages, and angiogenesis has been established so far. Furthermore, we do believe that this work provides new and interesting results, with Wnt signaling pathway emerging as an interesting target mediating beneficial outcomes during the inflammatory response undoubtedly linked to stroke pathology, where angiogenesis has been already proposed as a potential mechanism to promote recovery after the injury.
AB - Wnt3a is implicated in several key cellular processes and its expression has been reported in different cell types. Here, we report a novel function for Wnt3a in macrophages, whose exposure to this ligand shifts them towards a pro-angiogenic phenotype capable, under oxygen and glucose deprivation, of inducing in vitro tubular pattern structures in endothelial cells resembling capillary-like vasculature. These newly acquired angiogenetic features also include increased proliferation and migration and surprisingly, an increase in cell death. This work provides a new link between Wnt3a and macrophage-mediated angiogenesis under glucose and oxygen deprivation in vitro, which are worth further investigation in pathological conditions including stroke, where the stimulation of the angiogenic process might help to recovery after tissue injury Impact statement This work provides a new link between Wnt3a and macrophage-mediated angiogenesis under glucose and oxygen deprivation in vitro. Our results reveal how Wnt3a shifts macrophages towards a pro-angiogenic phenotype, which is able-in absence of both glucose and oxygen-of inducing angiogenesis in vitro, thus pointing to a synergy between the activation of the pathway and the hypoxia scenario. This work also demonstrates that modulation of cell death is key in order to explain the observed angiogenic effects. We consider all these findings of significant importance, since no connection between Wnt3a, macrophages, and angiogenesis has been established so far. Furthermore, we do believe that this work provides new and interesting results, with Wnt signaling pathway emerging as an interesting target mediating beneficial outcomes during the inflammatory response undoubtedly linked to stroke pathology, where angiogenesis has been already proposed as a potential mechanism to promote recovery after the injury.
KW - Journal Article
U2 - 10.1177/1535370217746392
DO - 10.1177/1535370217746392
M3 - Article
C2 - 29199847
SP - 1535370217746392
JO - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N. Y.)
SN - 0037-9727
ER -