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doi: 10.1242/10.1242/jcs.00128
Research Article |
1 Department of Anatomy and Cell Biology, The George Washington University
Medical School, Washington DC 20037, USA
2 Department of Ophthalmology, The George Washington University Medical School,
Washington DC 20037, USA
3 Division of Developmental and Newborn Biology, Department of Pediatrics,
Harvard Medical School, Boston, MA 02115, USA
4 Department of Pathology, The George Washington University Medical School,
Washington DC 20037, USA
* Author for correspondence (e-mail: mastepp{at}gwu.edu)
Accepted 22 August 2002
Mice lacking syndecan-1 are viable, fertile and have morphologically normal
skin, hair and ocular surface epithelia. While studying the response of these
mice to corneal epithelial and skin wounding, we identified defects in
epithelial cell proliferation and regulation of integrin expression. mRNA
profiling of corneal epithelial tissues obtained from wild-type and
syndecan-1-/- mice suggest that these defects result from
differences in overall gene transcription. In the cornea,
syndecan-1-/- epithelial cells migrate more slowly, show reduced
localization of 
9 integrin during closure of wounds and fail to
increase their proliferation rate 24 hours after wounding. In the skin, we did
not document a migration defect after full thickness wounds but did observe
cell proliferation delays and reduced localization of 9 integrin in the
syndecan-1-/- epidermis after dermabrasion. Despite increased cell
proliferation rates in the uninjured syndecan-1-/- epidermis and
the corneal epithelium, morphologically normal epithelial thickness is
maintained prior to injury; however, wounding is accompanied by prolonged
hypoplasia in both tissues. Analyses of integrin protein levels in extracts
from full thickness skin, revealed increased levels of 3 and 9
integrins both prior to injury and after hair removal in
syndecan-1-/- mice but no increase 2 days after dermabrasion. These
data for the first time show involvement of 9 integrin in skin wound
healing and demonstrate essential roles for syndecan-1 in mediating cell
proliferation and regulation of integrin expression in normal and wounded
epithelial tissues.
Key words: Syndecan-1, Wound healing, Cell proliferation, Integrins
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