The aim of the present study was to investigate the effect of testosterone on the modulation of cellular events associated with vascular homeostasis. In rat aortic strips, 5-20 min treatment with physiological concentrations of testosterone significantly increased nitric oxide (NO) production. The rapid action of the steroid was suppressed by the presence of an androgen receptor antagonist (flutamide). We obtained evidence that the enhancement in NO synthesis was dependent on the influx of calcium from extracellular medium, because in the presence of a calcium channel blocker (verapamil) the effect of testosterone was reduced. Using endothelial cell (EC) cultures, we demonstrated that androgen directly acts at the endothelial level. Chelerythrine or PD98059 compound completely suppressed the increase in NO production, suggesting that the mechanism of action of the steroid involves protein kinase C and mitogen-activated protein kinase pathways. It is known that endothelial NO released into the vascular lumen serves as an inhibitor of platelet activation and aggregation. We showed that testosterone inhibited platelet aggregation and this effect was dependent on endothelial NO synthesis. Indeed, the enhancement of NO production elicited by androgen was associated with EC growth. The steroid significantly increased DNA synthesis after 24 h of treatment, and this mitogenic action was blunted in the presence of NO synthase inhibitor N-nitro-L-arginine methyl ester. In summary, testosterone modulates vascular EC growth and platelet aggregation through its direct action on endothelial NO production.
Ionic substitution can affect essential physicochemical properties leading to a specific biological behavior upon implantation. Therefore, it has been proposed as a tool to increase the biological efficiency of calcium phosphate based materials. In the following study, we have evaluated the contribution of an important cation in nature, Mg, into the structure of previously studied biocompatible and biodegradable hydroxyapatite (HA) nanorods and its subsequent effect on its chemical, morphology, and bone mimetic articulation. Mg-substituted HA samples were synthesized by an aqueous wet-chemical precipitation method, followed by an hydrothermal treatment involving a Mg precursor that partially replace Ca ions into HA crystal lattice; Mg concentrations were modulated to obtain a nominal composition similar to that exists in calcified tissues. Hydrothermally synthesized Mg-substituted HA nanoparticles were characterized by X-ray powder diffraction, FT-NIR and EDX spectroscopies, field emission scanning and high resolution transmission electron microscopies (FE-SEM, H-TEM). Molecular modeling combining ab initio methods and power diffraction data were also performed. Results showed that Mg-substitution promoted the formation of calcium deficient HA (cdHA) where Mg replacement is energetically favored at Ca(1) position in a limited and specific amount directing the additional Mg toward the surface of the crystal. The control of Mg incorporation into HA nanorods gave rise to a tailored crystallinity degree, cell parameters, morphology, surface hydration, solubility, and degradation properties in a dose-replacement dependent manner. The obtained materials show qualities that conjugated together to drive an optimal in vitro cellular viability, spreading, and proliferation confirming their biocompatibility. In addition, an improved adhesion of osteoblast was evidenced after Mg-Ca substitution.
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