EGF regulates HAS-2 expression, controls epidermal thickness and stimulates keratinocyte migration
2002 (English)In: Hyaluronan, Vol 1: Chemical, Biochemical and Biological Aspects / [ed] Kennedy JF, Phillips GO, Williams PA, Hascall VC, Great Britain: Woodhead Publishing Limited, 2002, Vol. 1, 561-570 p.Conference paper (Refereed)
High concentrations of hyaluronan reside in the small space between the vital kertinocyte layers of human and animal epidermis and influence keratinocyte interactions, including growth, mobility and differentiation. We have previously found that the content of epidermal hyaluronan in human skin organ cultures is decreased and increased by cortisol and retinoic acid, and associated with enhanced and retarded terminal differentiation, respectively. To further substantiate this idea, we incubated epidermal keratinocytes with epidermal growth factor (EGF), and found a marked increase in hyaluronan synthesis which correlated with faster migration in an in vitro wounding assay of keratinocyte monolayers. EGF increased hyaluronan also in stratified, differentiated organotypic cultures, and increased the height of vital epidermis and reduced the thickness of the cornified layers, findings in line with an inhibition of terminal differentiation of keratinocytes. The stimulation of hyaluronan synthesis by EGF was due to upregulation of hyaluronan synthase 2 (HAS2) but not HAS1 or HAS3. A part of the EGF influence on the structure of epidermis, and on skin wound healing, is thus mediated through its control of HAS2 expression.
Place, publisher, year, edition, pages
Great Britain: Woodhead Publishing Limited, 2002. Vol. 1, 561-570 p.
Hyaluronan, keratinocytes, epidermis, migration, wound healing, epidermal growth factor
Cell and Molecular Biology Biochemistry and Molecular Biology Dermatology and Venereal Diseases
Research subject Biochemistry; cellforskning; Dermatology and Venerology
IdentifiersURN: urn:nbn:se:umu:diva-111589DOI: 10.1533/9781845693121.561ISBN: 1855735709OAI: oai:DiVA.org:umu-111589DiVA: diva2:871958