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Article: Ang1/Tie2/VE-Cadherin Signaling Regulates DPSCs in Vascular Maturation

TitleAng1/Tie2/VE-Cadherin Signaling Regulates DPSCs in Vascular Maturation
Authors
Keywordsdental pulp
human umbilical vein endothelial cells
pericytes
stem cells
transforming growth factor beta 1
vascular endothelial growth factor receptor 2
Issue Date2024
Citation
Journal of Dental Research, 2024, v. 103, n. 1, p. 101-110 How to Cite?
AbstractAdding dental pulp stem cells (DPSCs) to vascular endothelial cell–formed vessel-like structures can increase the longevity of these vessel networks. DPSCs display pericyte-like cell functions and closely assemble endothelial cells (ECs). However, the mechanisms of DPSC-derived pericyte-like cells in stabilizing the vessel networks are not fully understood. In this study, we investigated the functions of E-DPSCs, which were DPSCs isolated from the direct coculture of human umbilical vein endothelial cells (HUVECs) and DPSCs, and T-DPSCs, which were DPSCs treated by transforming growth factor beta 1 (TGF-β1), in stabilizing blood vessels in vitro and in vivo. A 3-dimensional coculture spheroid sprouting assay was conducted to compare the functions of E-DPSCs and T-DPSCs in vitro. Dental pulp angiogenesis in the severe combined immunodeficiency (SCID) mouse model was used to explore the roles of E-DPSCs and T-DPSCs in vascularization in vivo. The results demonstrated that both E-DPSCs and T-DPSCs possess smooth muscle cell–like cell properties, exhibiting higher expression of the mural cell–specific markers and the suppression of HUVEC sprouting. E-DPSCs and T-DPSCs inhibited HUVEC sprouting by activating TEK tyrosine kinase (Tie2) signaling, upregulating vascular endothelial (VE)–cadherin, and downregulating vascular endothelial growth factor receptor 2 (VEGFR2). In vivo study revealed more perfused and total blood vessels in the HUVEC + E-DPSC group, HUVEC + T-DPSC group, angiopoietin 1 (Ang1) pretreated group, and vascular endothelial protein tyrosine phosphatase (VE-PTP) inhibitor pretreated group, compared to HUVEC + DPSC group. In conclusion, these data indicated that E-DPSCs and T-DPSCs could stabilize the newly formed blood vessels and accelerate their perfusion. The critical regulating pathways are Ang1/Tie2/VE-cadherin and VEGF/VEGFR2 signaling.
Persistent Identifierhttp://hdl.handle.net/10722/341434
ISSN
2023 Impact Factor: 5.7
2023 SCImago Journal Rankings: 1.909
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, Y.-
dc.contributor.authorLin, S.-
dc.contributor.authorLiu, J.-
dc.contributor.authorChen, Q.-
dc.contributor.authorKang, J.-
dc.contributor.authorZhong, J.-
dc.contributor.authorHu, M.-
dc.contributor.authorBasabrain, M. S.-
dc.contributor.authorLiang, Y.-
dc.contributor.authorYuan, C.-
dc.contributor.authorZhang, C.-
dc.date.accessioned2024-03-13T08:42:47Z-
dc.date.available2024-03-13T08:42:47Z-
dc.date.issued2024-
dc.identifier.citationJournal of Dental Research, 2024, v. 103, n. 1, p. 101-110-
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/341434-
dc.description.abstractAdding dental pulp stem cells (DPSCs) to vascular endothelial cell–formed vessel-like structures can increase the longevity of these vessel networks. DPSCs display pericyte-like cell functions and closely assemble endothelial cells (ECs). However, the mechanisms of DPSC-derived pericyte-like cells in stabilizing the vessel networks are not fully understood. In this study, we investigated the functions of E-DPSCs, which were DPSCs isolated from the direct coculture of human umbilical vein endothelial cells (HUVECs) and DPSCs, and T-DPSCs, which were DPSCs treated by transforming growth factor beta 1 (TGF-β1), in stabilizing blood vessels in vitro and in vivo. A 3-dimensional coculture spheroid sprouting assay was conducted to compare the functions of E-DPSCs and T-DPSCs in vitro. Dental pulp angiogenesis in the severe combined immunodeficiency (SCID) mouse model was used to explore the roles of E-DPSCs and T-DPSCs in vascularization in vivo. The results demonstrated that both E-DPSCs and T-DPSCs possess smooth muscle cell–like cell properties, exhibiting higher expression of the mural cell–specific markers and the suppression of HUVEC sprouting. E-DPSCs and T-DPSCs inhibited HUVEC sprouting by activating TEK tyrosine kinase (Tie2) signaling, upregulating vascular endothelial (VE)–cadherin, and downregulating vascular endothelial growth factor receptor 2 (VEGFR2). In vivo study revealed more perfused and total blood vessels in the HUVEC + E-DPSC group, HUVEC + T-DPSC group, angiopoietin 1 (Ang1) pretreated group, and vascular endothelial protein tyrosine phosphatase (VE-PTP) inhibitor pretreated group, compared to HUVEC + DPSC group. In conclusion, these data indicated that E-DPSCs and T-DPSCs could stabilize the newly formed blood vessels and accelerate their perfusion. The critical regulating pathways are Ang1/Tie2/VE-cadherin and VEGF/VEGFR2 signaling.-
dc.languageeng-
dc.relation.ispartofJournal of Dental Research-
dc.subjectdental pulp-
dc.subjecthuman umbilical vein endothelial cells-
dc.subjectpericytes-
dc.subjectstem cells-
dc.subjecttransforming growth factor beta 1-
dc.subjectvascular endothelial growth factor receptor 2-
dc.titleAng1/Tie2/VE-Cadherin Signaling Regulates DPSCs in Vascular Maturation-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1177/00220345231210227-
dc.identifier.pmid38058134-
dc.identifier.scopuseid_2-s2.0-85179363440-
dc.identifier.volume103-
dc.identifier.issue1-
dc.identifier.spage101-
dc.identifier.epage110-
dc.identifier.eissn1544-0591-
dc.identifier.isiWOS:001115994600001-

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