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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,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 2001-02-01 do 2018-12-31
Medline Complete (EBSCOhost)
od 2000-01-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2001-02-01 do 2018-12-31
- MeSH
- antigeny CD44 biosyntéza genetika MeSH
- exprese genu MeSH
- glukuronosyltransferasa biosyntéza genetika MeSH
- hyaluronoglukosaminidasa biosyntéza genetika MeSH
- interleukin-6 biosyntéza MeSH
- interleukin-8 biosyntéza MeSH
- keratinocyty účinky léků metabolismus účinky záření MeSH
- kůže účinky léků metabolismus účinky záření MeSH
- kyselina hyaluronová metabolismus farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- toll-like receptor 2 biosyntéza genetika MeSH
- transformující růstový faktor beta biosyntéza MeSH
- ultrafialové záření MeSH
- viabilita buněk účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem 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.
Citace poskytuje Crossref.org
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- $a 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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