Linked Life Data

17666434

Source:http://linkedlifedata.com/resource/pubmed/id/17666434

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 16
pubmed:dateCreated
2007-8-10
pubmed:abstractText
We have reported previously that syndecan-1 (Sdc1)-null mice show delayed re-epithelialization after skin and corneal wounding. Here, we show that primary keratinocytes obtained from Sdc1-null mice and grown for 3-5 days in culture are more proliferative, more adherent and migrate more slowly than wt keratinocytes. However, the migration rates of Sdc1-null keratinocytes can be restored to wild-type levels by replating Sdc1-null keratinocytes onto tissue culture plates coated with fibronectin and collagen I, laminin (LN)-332 or onto the matrices produced by wild-type cells. Migration rates can also be restored by treating Sdc1-null keratinocytes with antibodies that block alpha6 or alphav integrin function, or with TGFbeta1. Antagonizing either beta1 integrin function using a function-blocking antibody or TGFbeta1 using a neutralizing antibody reduced wild-type keratinocyte migration more than Sdc1-null keratinocyte migration. Cultures of Sdc1-null keratinocytes accumulated less collagen than wild-type cultures but their matrices contained the same amount of LN-332. The Sdc1-null keratinocytes expressed similar total amounts of eight different integrin subunits but showed increased surface expression of alphavbeta6, alphavbeta8, and alpha6beta4 integrins compared with wild-type keratinocytes. Whereas wild-type keratinocytes increased their surface expression of alpha2beta1, alphavbeta6, alphavbeta8, and alpha6beta4 after treatment with TGFbeta1, Sdc1-null keratinocytes did not. Additional data from a dual-reporter assay and quantification of phosphorylated Smad2 show that TGFbeta1 signaling is constitutively elevated in Sdc1-null keratinocytes. Thus, our results identify TGFbeta1 signaling and Sdc1 expression as important factors regulating integrin surface expression, activity and migration in keratinocyte and provide new insight into the functions regulated by Sdc1.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9533
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
120
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2851-63
pubmed:meshHeading
pubmed-meshheading:17666434-Animals, pubmed-meshheading:17666434-Antibodies, pubmed-meshheading:17666434-Cell Adhesion, pubmed-meshheading:17666434-Cell Count, pubmed-meshheading:17666434-Cell Movement, pubmed-meshheading:17666434-Cell Shape, pubmed-meshheading:17666434-Extracellular Matrix, pubmed-meshheading:17666434-Gene Expression Regulation, pubmed-meshheading:17666434-Humans, pubmed-meshheading:17666434-Integrins, pubmed-meshheading:17666434-Keratinocytes, pubmed-meshheading:17666434-Keratins, pubmed-meshheading:17666434-Mice, pubmed-meshheading:17666434-Mice, Inbred BALB C, pubmed-meshheading:17666434-Models, Biological, pubmed-meshheading:17666434-RNA, Messenger, pubmed-meshheading:17666434-Signal Transduction, pubmed-meshheading:17666434-Syndecan-1, pubmed-meshheading:17666434-Time Factors, pubmed-meshheading:17666434-Transforming Growth Factor beta1
pubmed:year
2007
pubmed:articleTitle
Reduced migration, altered matrix and enhanced TGFbeta1 signaling are signatures of mouse keratinocytes lacking Sdc1.
pubmed:affiliation
Department of Anatomy and Cell Biology, George Washington University Medical School, Washington, DC 20037, USA. mastepp@gwu.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural, Research Support, N.I.H., Intramural