PI3K/AKT signaling drives titanium-induced angiogenic stimulus
Although osseointegration and clinical success of titanium (Ti)-implanted materials depend on neovascularization in the reactional peri-implant tissue, very little has been achieved considering the Ti-molecules release on the behavior of endothelial cells. To address this issue, we challenged endoth...
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| Veröffentlicht in: | Journal of materials science. Materials in medicine 2021, Vol.32 (1), p.18-18, Article 18 |
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| creator | Martins, Bruna Rodrigues Pinto, Thais Silva da Costa Fernandes, Célio Junior Bezerra, Fábio Zambuzzi, Willian Fernando |
| description | Although osseointegration and clinical success of titanium (Ti)-implanted materials depend on neovascularization in the reactional peri-implant tissue, very little has been achieved considering the Ti-molecules release on the behavior of endothelial cells. To address this issue, we challenged endothelial cells (HUVECs) with Ti-enriched medium obtained from two types of commercial titanium surfaces [presenting or not dual-acid etching (DAE)] up to 72 h to allow molecular machinery analysis. Our data show that the Ti-enriched medium provokes significant stimulus of angiogenesis-related machinery in endothelial cells by upexpressing VEGFR1, VEGFR2, VEGF, eNOS, and iNOS genes, while the PI3K/Akt signaling pathway was also significantly enhanced. As PI3K/AKT signaling was related to angiogenesis in response to vascular endothelial growth factor (VEGF), we addressed the importance of PI3K/Akt upon Ti-enriched medium responses by concomitantly treating the cells with wortmannin, a well-known PI3K inhibitor. Wortmannin suppressed the angiogenic factors, because VEGF, VEGFR1, and eNOS genes were downregulated in those cells, highlighting the importance of PI3K/AKT signaling on driving angiogenic phenotype and angiogenesis performance within the peri-implant tissue reaction. In conjunction, these data reinforce that titanium-implantable devices modify the metabolism of surrounding cells, such as endothelial cells, probably coupling osteogenesis and angiogenesis processes in peri-implant tissue and then contributing to successfully osseointegration of biomedical titanium-based devices. |
| doi_str_mv | 10.1007/s10856-020-06473-8 |
| format | Article |
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To address this issue, we challenged endothelial cells (HUVECs) with Ti-enriched medium obtained from two types of commercial titanium surfaces [presenting or not dual-acid etching (DAE)] up to 72 h to allow molecular machinery analysis. Our data show that the Ti-enriched medium provokes significant stimulus of angiogenesis-related machinery in endothelial cells by upexpressing VEGFR1, VEGFR2, VEGF, eNOS, and iNOS genes, while the PI3K/Akt signaling pathway was also significantly enhanced. As PI3K/AKT signaling was related to angiogenesis in response to vascular endothelial growth factor (VEGF), we addressed the importance of PI3K/Akt upon Ti-enriched medium responses by concomitantly treating the cells with wortmannin, a well-known PI3K inhibitor. Wortmannin suppressed the angiogenic factors, because VEGF, VEGFR1, and eNOS genes were downregulated in those cells, highlighting the importance of PI3K/AKT signaling on driving angiogenic phenotype and angiogenesis performance within the peri-implant tissue reaction. In conjunction, these data reinforce that titanium-implantable devices modify the metabolism of surrounding cells, such as endothelial cells, probably coupling osteogenesis and angiogenesis processes in peri-implant tissue and then contributing to successfully osseointegration of biomedical titanium-based devices.</description><identifier>ISSN: 0957-4530</identifier><identifier>EISSN: 1573-4838</identifier><identifier>DOI: 10.1007/s10856-020-06473-8</identifier><identifier>PMID: 33506378</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Angiogenesis ; Biomaterials ; Biomaterials Synthesis and Characterization ; Biomedical Engineering and Bioengineering ; Biomedical materials ; Ceramics ; Chemistry and Materials Science ; Composites ; Coupling (molecular) ; Electronic devices ; Endothelial cells ; Enrichment ; Etching ; Genes ; Glass ; Growth factors ; Materials Science ; Metabolism ; Molecular machines ; Natural Materials ; Nitric oxide ; Nitric-oxide synthase ; Osseointegration ; Osteogenesis ; Phenotypes ; Polymer Sciences ; Regenerative Medicine/Tissue Engineering ; Signal transduction ; Signaling ; Surfaces and Interfaces ; Surgical implants ; Thin Films ; Tissues ; Titanium ; Vascular endothelial growth factor ; Vascularization ; Wortmannin</subject><ispartof>Journal of materials science. Materials in medicine, 2021, Vol.32 (1), p.18-18, Article 18</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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Materials in medicine</title><addtitle>J Mater Sci: Mater Med</addtitle><addtitle>J Mater Sci Mater Med</addtitle><description>Although osseointegration and clinical success of titanium (Ti)-implanted materials depend on neovascularization in the reactional peri-implant tissue, very little has been achieved considering the Ti-molecules release on the behavior of endothelial cells. To address this issue, we challenged endothelial cells (HUVECs) with Ti-enriched medium obtained from two types of commercial titanium surfaces [presenting or not dual-acid etching (DAE)] up to 72 h to allow molecular machinery analysis. Our data show that the Ti-enriched medium provokes significant stimulus of angiogenesis-related machinery in endothelial cells by upexpressing VEGFR1, VEGFR2, VEGF, eNOS, and iNOS genes, while the PI3K/Akt signaling pathway was also significantly enhanced. As PI3K/AKT signaling was related to angiogenesis in response to vascular endothelial growth factor (VEGF), we addressed the importance of PI3K/Akt upon Ti-enriched medium responses by concomitantly treating the cells with wortmannin, a well-known PI3K inhibitor. Wortmannin suppressed the angiogenic factors, because VEGF, VEGFR1, and eNOS genes were downregulated in those cells, highlighting the importance of PI3K/AKT signaling on driving angiogenic phenotype and angiogenesis performance within the peri-implant tissue reaction. In conjunction, these data reinforce that titanium-implantable devices modify the metabolism of surrounding cells, such as endothelial cells, probably coupling osteogenesis and angiogenesis processes in peri-implant tissue and then contributing to successfully osseointegration of biomedical titanium-based devices.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Biomaterials</subject><subject>Biomaterials Synthesis and Characterization</subject><subject>Biomedical Engineering and Bioengineering</subject><subject>Biomedical materials</subject><subject>Ceramics</subject><subject>Chemistry and Materials Science</subject><subject>Composites</subject><subject>Coupling (molecular)</subject><subject>Electronic devices</subject><subject>Endothelial cells</subject><subject>Enrichment</subject><subject>Etching</subject><subject>Genes</subject><subject>Glass</subject><subject>Growth 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Materials in medicine</jtitle><stitle>J Mater Sci: Mater Med</stitle><addtitle>J Mater Sci Mater Med</addtitle><date>2021</date><risdate>2021</risdate><volume>32</volume><issue>1</issue><spage>18</spage><epage>18</epage><pages>18-18</pages><artnum>18</artnum><issn>0957-4530</issn><eissn>1573-4838</eissn><abstract>Although osseointegration and clinical success of titanium (Ti)-implanted materials depend on neovascularization in the reactional peri-implant tissue, very little has been achieved considering the Ti-molecules release on the behavior of endothelial cells. To address this issue, we challenged endothelial cells (HUVECs) with Ti-enriched medium obtained from two types of commercial titanium surfaces [presenting or not dual-acid etching (DAE)] up to 72 h to allow molecular machinery analysis. Our data show that the Ti-enriched medium provokes significant stimulus of angiogenesis-related machinery in endothelial cells by upexpressing VEGFR1, VEGFR2, VEGF, eNOS, and iNOS genes, while the PI3K/Akt signaling pathway was also significantly enhanced. As PI3K/AKT signaling was related to angiogenesis in response to vascular endothelial growth factor (VEGF), we addressed the importance of PI3K/Akt upon Ti-enriched medium responses by concomitantly treating the cells with wortmannin, a well-known PI3K inhibitor. Wortmannin suppressed the angiogenic factors, because VEGF, VEGFR1, and eNOS genes were downregulated in those cells, highlighting the importance of PI3K/AKT signaling on driving angiogenic phenotype and angiogenesis performance within the peri-implant tissue reaction. In conjunction, these data reinforce that titanium-implantable devices modify the metabolism of surrounding cells, such as endothelial cells, probably coupling osteogenesis and angiogenesis processes in peri-implant tissue and then contributing to successfully osseointegration of biomedical titanium-based devices.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33506378</pmid><doi>10.1007/s10856-020-06473-8</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-4149-5965</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Angiogenesis Biomaterials Biomaterials Synthesis and Characterization Biomedical Engineering and Bioengineering Biomedical materials Ceramics Chemistry and Materials Science Composites Coupling (molecular) Electronic devices Endothelial cells Enrichment Etching Genes Glass Growth factors Materials Science Metabolism Molecular machines Natural Materials Nitric oxide Nitric-oxide synthase Osseointegration Osteogenesis Phenotypes Polymer Sciences Regenerative Medicine/Tissue Engineering Signal transduction Signaling Surfaces and Interfaces Surgical implants Thin Films Tissues Titanium Vascular endothelial growth factor Vascularization Wortmannin |
| title | PI3K/AKT signaling drives titanium-induced angiogenic stimulus |
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