File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Sema4d/plexinb1 Promotes Endothelial Differentiation Of Dental Pulp Stem Cells Via Activation Of Akt And Erk1/2 Signaling.

TitleSema4d/plexinb1 Promotes Endothelial Differentiation Of Dental Pulp Stem Cells Via Activation Of Akt And Erk1/2 Signaling.
Authors
KeywordsAKT
DPSCs
endothelial differentiation
ERK1/2
Sema4D
Issue Date2019
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503
Citation
Journal of Cellular Biochemistry, 2019, v. 120 n. 8, p. 13614-13624 How to Cite?
AbstractInducing of dental pulp stem cells (DPSCs) into endothelial cells (ECs) to prevascularize pulp tissue constructs may offer a novel and viable approach for enhancing pulp regeneration. However, there are numerous challenges in current methods for the acquisition of sufficient translational ECs. It was known that Sema4D/PlexinB1 signaling exerts profound effects on enhancing vascular endothelial growth factor (VEGF) secretion and angiogenesis. Whether Sema4D/PlexinB1 could regulate endothelial differentiation of DPSCs is not yet investigated. In this study, when DPSCs were treated with Sema4D (2 μg/mL), ECs-specific (VEGFR1, VEGFR2, CD31, and vWF), and angiogenic genes and proteins were significantly upregulated. The induced ECs exhibited similar endothelial vessel formation ability to that of human umbilical vein endothelial cells (HUVECs). Furthermore, phosphorylation of AKT increased dramatically within 5 minutes (from 0.93 to 21.8), while p-ERK1/2 was moderately elevated (from 0.94 to 2.65). In summary, our results demonstrated that Sema4D/PlexinB1 signaling induces endothelial differentiation of DPSCs. The interactions of Sema4D, VEGF, ANGPTL4, ANG1, and HIF-1α may play a crucial role in mediating the differentiation process. © 2019 Wiley Periodicals, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/275688
ISSN
2017 Impact Factor: 2.959
2015 SCImago Journal Rankings: 1.520
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZou, T-
dc.contributor.authorJiang, S-
dc.contributor.authorDissanayaka, WL-
dc.contributor.authorHeng, BC-
dc.contributor.authorXu, J-
dc.contributor.authorGong, T-
dc.contributor.authorHuang, X-
dc.contributor.authorZhang, C-
dc.date.accessioned2019-09-10T02:47:38Z-
dc.date.available2019-09-10T02:47:38Z-
dc.date.issued2019-
dc.identifier.citationJournal of Cellular Biochemistry, 2019, v. 120 n. 8, p. 13614-13624-
dc.identifier.issn0730-2312-
dc.identifier.urihttp://hdl.handle.net/10722/275688-
dc.description.abstractInducing of dental pulp stem cells (DPSCs) into endothelial cells (ECs) to prevascularize pulp tissue constructs may offer a novel and viable approach for enhancing pulp regeneration. However, there are numerous challenges in current methods for the acquisition of sufficient translational ECs. It was known that Sema4D/PlexinB1 signaling exerts profound effects on enhancing vascular endothelial growth factor (VEGF) secretion and angiogenesis. Whether Sema4D/PlexinB1 could regulate endothelial differentiation of DPSCs is not yet investigated. In this study, when DPSCs were treated with Sema4D (2 μg/mL), ECs-specific (VEGFR1, VEGFR2, CD31, and vWF), and angiogenic genes and proteins were significantly upregulated. The induced ECs exhibited similar endothelial vessel formation ability to that of human umbilical vein endothelial cells (HUVECs). Furthermore, phosphorylation of AKT increased dramatically within 5 minutes (from 0.93 to 21.8), while p-ERK1/2 was moderately elevated (from 0.94 to 2.65). In summary, our results demonstrated that Sema4D/PlexinB1 signaling induces endothelial differentiation of DPSCs. The interactions of Sema4D, VEGF, ANGPTL4, ANG1, and HIF-1α may play a crucial role in mediating the differentiation process. © 2019 Wiley Periodicals, Inc.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/35503-
dc.relation.ispartofJournal of Cellular Biochemistry-
dc.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Postprint This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectAKT-
dc.subjectDPSCs-
dc.subjectendothelial differentiation-
dc.subjectERK1/2-
dc.subjectSema4D-
dc.titleSema4d/plexinb1 Promotes Endothelial Differentiation Of Dental Pulp Stem Cells Via Activation Of Akt And Erk1/2 Signaling.-
dc.typeArticle-
dc.identifier.emailJiang, S: jshan@hku.hk-
dc.identifier.emailDissanayaka, WL: warunad@hku.hk-
dc.identifier.emailZhang, C: zhangcf@hku.hk-
dc.identifier.authorityDissanayaka, WL=rp02216-
dc.identifier.authorityZhang, C=rp01408-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jcb.28635-
dc.identifier.pmid30937968-
dc.identifier.scopuseid_2-s2.0-85067281112-
dc.identifier.hkuros302706-
dc.identifier.volume120-
dc.identifier.issue8-
dc.identifier.spage13614-
dc.identifier.epage13624-
dc.identifier.isiWOS:000471718300148-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats