<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>7</volume><submitter>Janjic K</submitter><pubmed_abstract>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)-1?, tumor necrosis factor (TNF)? or transforming growth factor (TGF)?, 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. TNF?, TGF?, L-MIM, or combined treatment did not modulate Sost and Dkk-1. IL-1? 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-1? 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.</pubmed_abstract><journal>Frontiers in bioengineering and biotechnology</journal><pagination>430</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6927906</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Influence of Pro-Inflammatory Factors on Sclerostin and Dickkopf-1 Production in Human Dental Pulp Cells Under Hypoxic Conditions.</pubmed_title><pmcid>PMC6927906</pmcid><pubmed_authors>Moritz A</pubmed_authors><pubmed_authors>Janjic K</pubmed_authors><pubmed_authors>Samiei M</pubmed_authors><pubmed_authors>Agis H</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Influence of Pro-Inflammatory Factors on Sclerostin and Dickkopf-1 Production in Human Dental Pulp Cells Under Hypoxic Conditions.</name><description>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)-1?, tumor necrosis factor (TNF)? or transforming growth factor (TGF)?, 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. TNF?, TGF?, L-MIM, or combined treatment did not modulate Sost and Dkk-1. IL-1? 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-1? 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.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2020-11-20T10:04:15Z</modification><creation>2020-05-22T07:37:21Z</creation></dates><accession>S-EPMC6927906</accession><cross_references><pubmed>31921831</pubmed><doi>10.3389/fbioe.2019.00430</doi></cross_references></HashMap>