Sclerostin (Sost) and dickkopf (Dkk)-1 are inhibitors of the Wnt signaling pathway that plays a role in regenerative processes.
Hypoxia-based strategies are used for regenerative approaches, but the influence of
hypoxia on Sost and Dkk-1 production in a pro-inflammatory environment is unclear. The aim of this study was to assess if pro-inflammatory molecules have an influence on Sost and Dkk-1 production in dental pulp cells (DPC) under normoxia and
hypoxia. Human DPC were treated with
interleukin (IL)-1β,
tumor necrosis factor (TNF)α or
transforming growth factor (TGF)β, with L-
mimosine (L-MIM) or
hypoxia or a combination. Sost and Dkk-1
mRNA and
protein levels were measured with qPCR and western blot, respectively. TNFα, TGFβ, L-MIM, or combined treatment did not modulate Sost and Dkk-1. IL-1β downregulated Sost at the
mRNA level.
Hypoxia alone and together with inflammatory markers downregulated Dkk-1 at the
mRNA level. Sost and Dkk-1
protein production was below the detection limit. In conclusion, there is a differential effect of
hypoxia and IL-1β on the
mRNA production of Sost and Dkk-1. Pro-inflammatory molecules do not further modulate the effects of L-MIM or
hypoxia on Sost and Dkk-1 production in DPC.