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Cdc42 and p190RhoGA...
Cdc42 and p190RhoGAP activation by CCN2 regulates cell spreading and polarity and induces actin disassembly in migrating keratinocytes
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- Kiwanuka, Elizabeth, 1983- (författare)
- Uppsala universitet,Plastikkirurgi,Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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- Lee, Cameron C.Y. (författare)
- Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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- Hackl, Florian (författare)
- Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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- Caterson, Edward J. (författare)
- Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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- Junker, Johan (författare)
- Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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- Gerdin, Bengt (författare)
- Uppsala universitet,Plastikkirurgi
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- Eriksson, Elof (författare)
- Division of Plastic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
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(creator_code:org_t)
- 2014-09-03
- 2016
- Engelska.
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Ingår i: International Wound Journal. - : Wiley. - 1742-4801 .- 1742-481X. ; 13:3, s. 372-381
- Relaterad länk:
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https://www.ncbi.nlm...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Cell migration requires spatiotemporal integration of signals that regulate cytoskeletal dynamics. In response to a migration-promoting agent, cells begin to polarise and extend protrusions in the direction of migration. These cytoskeletal rearrangements are orchestrated by a variety of proteins, including focal adhesion kinase (FAK) and the Rho family of GTPases. CCN2, also known as connective tissue growth factor, has emerged as a regulator of cell migration but the mechanism by which CCN2 regulates keratinocyte function is not well understood. In this article, we sought to elucidate the basicmechanism of CCN2-induced cellmigration in human keratinocytes. Immunohistochemical staining was used to demonstrate that treatment with CCN2 induces a migratory phenotype through actin disassembly, spreading of lamellipodia and re-orientation of the Golgi. In vitro assays were used to show that CCN2-induced cell migration is dependent on FAK, RhoA and Cdc42, but independent of Rac1. CCN2-treated keratinocytes displayed increased Cdc42 activity and decreased RhoA activity up to 12 hours post-treatment, with upregulation of p190RhoGAP. An improved understanding of how CCN2 regulates cell migration may establish the foundation for future therapeutics in fibrotic and neoplastic diseases.
Nyckelord
- RhoGTPase
- Actin
- CCN2
- CTGF
- Keratinocyte migration
- Plastic Surgery
- Plastikkirurgi
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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