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Hyaluronan minimizes effects of UV irradiation on human keratinocytes
M. Hašová, T. Crhák, B. Safránková, J. Dvořáková, T. Muthný, V. Velebný, L. Kubala,
Language English Country Germany
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
ProQuest Central
from 2001-02-01 to 2018-12-31
Medline Complete (EBSCOhost)
from 2000-01-01 to 1 year ago
Health & Medicine (ProQuest)
from 2001-02-01 to 2018-12-31
- MeSH
- Hyaluronan Receptors biosynthesis genetics MeSH
- Gene Expression MeSH
- Glucuronosyltransferase biosynthesis genetics MeSH
- Hyaluronoglucosaminidase biosynthesis genetics MeSH
- Interleukin-6 biosynthesis MeSH
- Interleukin-8 biosynthesis MeSH
- Keratinocytes drug effects metabolism radiation effects MeSH
- Skin drug effects metabolism radiation effects MeSH
- Hyaluronic Acid metabolism pharmacology MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- Toll-Like Receptor 2 biosynthesis genetics MeSH
- Transforming Growth Factor beta biosynthesis MeSH
- Ultraviolet Rays MeSH
- Cell Survival drug effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Exposure to ultraviolet (UV) irradiation has detrimental effects on skin accompanied by the increased metabolism of hyaluronan (HA), a linear polysaccharide important for the normal physiological functions of skin. In this study, the modulation of human keratinocyte response to UVB irradiation by HA (970 kDa) was investigated. Immortalized human keratinocytes (HaCaT) were irradiated by a single dose of UVB and immediately treated with HA for 6 and 24 h. The irradiation induced a significant decrease in the gene expression of CD44 and toll-like receptor 2 6 h after irradiation. The expressions of other HA receptors, including toll-like receptor 4 and the receptor for HA-mediated motility, were not detected in either the control or UVB-irradiated or HA-treated HaCaT cells. UVB irradiation induced a significant decrease in the gene expression of HA synthase-2 and hyaluronidase-2 6 h after irradiation. The expressions of HA synthase-3 and hyaluronidase-3 were not significantly modulated by UV irradiation. Interestingly, HA treatment did not significantly modulate any of these effects. In contrast, HA significantly suppressed UVB-induced pro-inflammatory cytokine release including interleukin-6 and interleukin-8. Similarly, HA treatment reduced the UVB-mediated production of transforming growth factor β1. HA treatment also significantly reduced the UV irradiation-mediated release of soluble CD44 into the media. Finally, HA partially, but significantly, suppressed the UVB-induced decrease in cell viability. Data indicate that HA had significant protective effects for HaCaT cells against UVB irradiation.
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