INVESTIGADORES
BALAÑA Maria Eugenia
congresos y reuniones científicas
Título:
Angiogenic capabilities driven by dermal papilla cells and their modulation by androgen action
Autor/es:
PROIETTI, CECILIA JAZMIN; GAITAN, ANA MARÍA; CERUTI, JULIETA MARÍA; LEIROS, GUSTAVO JOSÉ; BALAÑA , MARÍA EUGENIA
Lugar:
Lisboa
Reunión:
Congreso; 53rd ANNUAL ESDR MEETING; 2024
Resumen:
The onset of the anagen phase involves the migration of HFSCs from the bulge to the base of the bulb and their differentiation into matrix cells. Anagen initiation requires the stimulation of a new vascular network to support the growth phase. DPCs are implicated in both embryonic neogenesis and the hair follicle cycle. Therefore, DPC signaling plays a pivotal role in both processes. We have demonstrated that androgens decrease DPC inductivity on HFSC differentiation. Conversely, we have shown that culturing DPCs as spheres promotes the migration of endothelial cells and vascular network formation, as well as the expression of proangiogenic factors. In this study, we aimed to evaluate the action of androgens on the expression of angiogenic factors and investigate whether the increased angiogenic potential of DPCs cultured as spheres can be retained after successive passages. Our results indicate that androgens negatively regulate the expression of VEGF and FGF in DPCs cultured as spheres. On the other hand, the expression of both angiogenic factors increases when DPCs are cultured as spheres. Even though this increase is lost when DPCs are subsequently cultured as monolayer, culturing them as spheres restores the higher expression. These results suggest that passaged spheres retain an increased level of the main angiogenic factors despite DPC amplification as monolayer. We can speculate about the relevance of these results for translational medicine when large amounts of DPCs are needed. These results, combined with previous findings from the laboratory, allow us to speculate that androgens may alter the onset of anagen both by impairing HFSC differentiation and by generating an insufficient vascular network to support the growth phase