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001-es BibID:	BIBFORM086257
035-os BibID:	(WOS)000485661500556
Első szerző:	Fidrus Eszter (biotechnológus)
Cím:	Time-dependence of UVB induced cellular mechanisms in cultured human keratinocytes / E. Fidrus, G. Boros, C. Hegedűs, E. A. Janka, G. Emri, K. Karikó, É. Remenyik
Dátum:	2019
ISSN:	0022-202X 1523-1747
Megjegyzések:	UVB-induced cyclobutane pyrimidine dimers (CPDs) are considered to be the main cause of acute sunburn and epidermal carcinogenesis. In humans, these lesions are repaired by nucleotide excision repair, but marsupials and lower organisms present photolyase enzyme which rapidly removes CPDs in a visible light-dependent process (photoreactivation). Previously we established an in vitro pseudouridin-modified mRNA encoding CPD-specific photolyase transfection on human keratinocyte cell lines, which was proved to be a proper method to avoid UVB-induced apoptosis. According to clinical experiences, there is a need for a treatment to diminish the deleterious effects of sunburn when UVB injury has already occurred and the first symptoms appear. Our aim was to determine the time interval after UVB exposure when keratinocyte apoptosis is still preventable. Normal human epidermal keratinocytes were transfected with lipofectamine-complexed, in vitro transcribed mRNA encoding CPD-specific photolyase. Cells were irradiated with 60 mJ/cm2 UVB. At 0, 6, 8 or 12 hours after UVB cells were either exposed to visible light (photoreactivation) or kept in the dark. Viability was measured by Annexin V and propidium iodide dual staining followed by flow cytometry, the relative amount of intracellular CPDs was analyzed by CPD-specific ELISA. Photolyase-mediated CPD removal restored cell viability close to the baseline conditions 0 to 6 hours after UVB treatment. The effect of CPD removal on keratinocyte survival began to decrease 8 hours after the UVB damage. In mRNA-transfected and photoreactivated cells 80% of CPDs were removed at 6 hours post-irradiation. 8 to 12 hours after UVB 40-60% of the CPDs were eliminated. Our results suggest that UV-induced keratinocyte apoptosis can be prevented within 6-8 hours after the UVB injury by the elimination of CPD photolesions. After that point the effect of CPD removal on cell viability is less feasible.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok poszter folyóiratcikk
Megjelenés:	Journal of Investigative Dermatology. - 139 : 9 (2019), p. S311. -
További szerzők:	Boros Gábor Hegedűs Csaba (1988-) (molekuláris biológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Karikó Katalin (1955-) (biológus, biokémikus) Remenyik Éva (1956-) (bőrgyógyász)
Pályázati támogatás:	K120206 OTKA GINOP-2.3.2-15-2016-00005 GINOP
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM086255
035-os BibID:	(WOS)000485661500557
Első szerző:	Fidrus Eszter (biotechnológus)
Cím:	Enhanced UVA-induced cyclobutane pyrimidine dimer formation by silymarin without increased mutagenesis in cultured epithelial cells / E. Fidrus, P. Fehér, C. Hegedus, E. A. Janka, G. Paragh, I. Bácskay, É. Remenyik
Dátum:	2019
ISSN:	0022-202X 1523-1747
Megjegyzések:	Ultraviolet B radiation (UVB) causes direct DNA damage by inducing the formation of cyclobutane pyrimidine dimers (CPDs). These photolesions lead to diverse cellular effects, but their involvement in the regulation of mitochondrial function is unexplored. Here, we characterized the impact of UVB-induced DNA damage on the mitochondria using our established model system, in which human keratinocytes are transfected with methylpseudouridine- modified mRNA encoding CPD-photolyase. Our results demonstrate that CPD removal by photoactivated CPD-photolyase in HaCaT cells reduces PARP activation and bulk autophagy after UVB exposure. Moreover, the CPD-photolyase prevents G2/M cell cycle arrest and restores cell viability. Removal of CPD also prevented the UVB-mediated increase in mitochondrial mass, mitochondrial biogenesis and morphological changes of mitochondria. Alterations in mitochondrial number, area, shape descriptors and expressional changes of fusion proteins indicated that photoactivation of CPD-photolyase can prevent UVBinduced mitochondrial fusion. As a result of photolyase activity mitochondrial membrane potential, superoxide production, glycolysis and oxidative phosphorylation were all reduced to baseline levels.We also demonstrated that following removal of CPDs the expression of the upstream regulators of oxidative phosphorylation was decreased, thus suggesting that UVBinitiated DNA damage likely induces nucleus-to-mitochondria signaling. In conclusion, delivery of CPD-photolyase mRNA into cultured human keratinocytes provides a protective effect not only against DNA damage but also prevents morphological and functional changes of mitochondria after UVB exposure.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok poszter folyóiratcikk
Megjelenés:	Journal of Investigative Dermatology. - 139 : 9 (2019), p. S311. -
További szerzők:	Fehér Pálma (1976-) (gyógyszerész) Hegedűs Csaba (1988-) (molekuláris biológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Paragh György Jr. (1978-) (bőrgyógyász) Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Remenyik Éva (1956-) (bőrgyógyász)
Pályázati támogatás:	K120206 OTKA GINOP-2.3.2-15-2016-00005 GINOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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