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Article: Epac Activation Regulates Human Mesenchymal Stem Cells Migration and Adhesion

TitleEpac Activation Regulates Human Mesenchymal Stem Cells Migration and Adhesion
Authors
Issue Date2016
PublisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.com
Citation
Stem Cells, 2016, v. 34 n. 4, p. 948-959 How to Cite?
AbstractHow to enhance the homing of human mesenchymal stem cells (hMSCs) to the target tissues remains a clinical challenge nowadays. To overcome this barrier, the mechanism responsible for the hMSCs migration and engraftment has to be defined. Currently, the exact mechanism involved in migration and adhesion of hMSCs remains unknown. Exchange protein directly activated by cAMP (Epac), a novel protein discovered in cAMP signaling pathway, may have a potential role in regulating cells adhesion and migration by triggering the downstream Rap family signaling cascades. However, the exact role of Epac in cells homing is elusive. Our study evaluated the role of Epac in the homing of hMSCs. We confirmed that hMSCs expressed functional Epac and its activation enhanced the migration and adhesion of hMSCs significantly. The Epac activation was further found to be contributed directly to the chemotactic responses induced by stromal cell derived factor-1 (SDF-1) which is a known chemokine in regulating hMSCs homing. These findings suggested Epac is connected to the SDF-1 signaling cascades. In conclusion, our study revealed that Epac plays a role in hMSCs homing by promoting adhesion and migration. Appropriate manipulation of Epac may enhance the homing of hMSCs and facilitate their future clinical applications.
Persistent Identifierhttp://hdl.handle.net/10722/230570
ISSN
2015 Impact Factor: 5.902
2015 SCImago Journal Rankings: 3.438

 

DC FieldValueLanguage
dc.contributor.authorYu, JL-
dc.contributor.authorDeng, R-
dc.contributor.authorChung, SK-
dc.contributor.authorChan, GCF-
dc.date.accessioned2016-08-23T14:17:48Z-
dc.date.available2016-08-23T14:17:48Z-
dc.date.issued2016-
dc.identifier.citationStem Cells, 2016, v. 34 n. 4, p. 948-959-
dc.identifier.issn1066-5099-
dc.identifier.urihttp://hdl.handle.net/10722/230570-
dc.description.abstractHow to enhance the homing of human mesenchymal stem cells (hMSCs) to the target tissues remains a clinical challenge nowadays. To overcome this barrier, the mechanism responsible for the hMSCs migration and engraftment has to be defined. Currently, the exact mechanism involved in migration and adhesion of hMSCs remains unknown. Exchange protein directly activated by cAMP (Epac), a novel protein discovered in cAMP signaling pathway, may have a potential role in regulating cells adhesion and migration by triggering the downstream Rap family signaling cascades. However, the exact role of Epac in cells homing is elusive. Our study evaluated the role of Epac in the homing of hMSCs. We confirmed that hMSCs expressed functional Epac and its activation enhanced the migration and adhesion of hMSCs significantly. The Epac activation was further found to be contributed directly to the chemotactic responses induced by stromal cell derived factor-1 (SDF-1) which is a known chemokine in regulating hMSCs homing. These findings suggested Epac is connected to the SDF-1 signaling cascades. In conclusion, our study revealed that Epac plays a role in hMSCs homing by promoting adhesion and migration. Appropriate manipulation of Epac may enhance the homing of hMSCs and facilitate their future clinical applications.-
dc.languageeng-
dc.publisherAlphaMed Press, Inc. The Journal's web site is located at http://www.stemcells.com-
dc.relation.ispartofStem Cells-
dc.titleEpac Activation Regulates Human Mesenchymal Stem Cells Migration and Adhesion -
dc.typeArticle-
dc.identifier.emailDeng, R: rxdeng@hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.authorityChan, GCF=rp00431-
dc.identifier.doi10.1002/stem.2264-
dc.identifier.hkuros261523-
dc.identifier.volume34-
dc.identifier.issue4-
dc.identifier.spage948-
dc.identifier.epage959-
dc.publisher.placeUnited States-

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