CCL

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1.

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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2.

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
Borító:

3.

001-es BibID:BIBFORM086253
035-os BibID:BIBFORM086253
Első szerző:Gellén Emese (bőrgyógyász)
Cím:642 Efficacy and photorejuvenation effect of conventional photodynamic therapy (PDT) and Er:YAG (erbium:yttrium-aluminium-garnet) ablative fractional laser - assisted PDT in multiple actinic keratosis / E. Gellén, E. Fidrus, E. A. Janka, B. Barta, G. Emri, É. Remenyik
Dátum:2017
ISSN:0022-202X 1523-1747
Megjegyzések:Actinic keratosis is the precancerous lesion of squamous cell carcinoma. Their multiple appearance on one area reflects field cancerization. Therefore active treatment of the field is necessary to avoid the development of incidental squamous cell carcinoma. Conventional photodynamic therapy (PDT) is a widely used therapeutic method for actinic keratosis. Er:YAG (erbium:yttrium-aluminium-garnet) ablative fractional laser (AFL) - assisted PDT is used to increase the therapeutic efficacy of conventional PDT. The aim of this study was to assess the differences between conventional PDT and Er:YAG - assisted PDT both in efficacy and rejuvenation effect. To investigate the therapeutic efficiency, sixteen patients with actinic keratosis and chronic sun-damaged skin were irradiated with wIRA lamp on the half side of the skin involved in actinic keratosis e after 20% 5-aminolevulinic acid was applied as photosensitizer. The other side of the skin was pre-treated with Er:YAG-AFL before 5-ALA. 24/ 48 hours and 3 months after the treatment biopsy samples were taken to measure the degree of the keratinocyte dysplasia compared to the control (untreated) samples. P53 mutant keratinocytes were detected with immunohistochemical staining. The number and grade of actinic keratosis and the objective signs of photoaging was also assessed. In our hands, both conventional PDT and Er:YAG-AFL - assisted PDT led to great reduction in the number of actinic keratosis, and this decrease was significantly higher in the case of Er:YAG-AFL PDT. Both improved global photoaging, but we found no significant differences between the two methods. According to the immunohistochemical staining, both decreased the number of p53 mutant keratinocytes in the epidermis. We found no significant differences in the therapeutic efficiency between Er:YAG-AFL PDT and conventional PDT regarding clinical and immunohistochemical evaluation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok poszter
folyóiratcikk
Megjelenés:Journal Of Investigative Dermatology. - 137 : 10 (2017), p. S302-. -
További szerzők:Fidrus Eszter (1992-) (biotechnológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Barta Bianka Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Remenyik Éva (1956-) (bőrgyógyász)
Pályázati támogatás:K1120206
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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4.

001-es BibID:BIBFORM086259
035-os BibID:(WOS)000485661500545
Első szerző:Hegedűs Csaba (biokémikus, molekuláris biológus)
Cím:In vitro delivery of CPD-specific photolyase-encoding mRNA prevents UVB-induced mitochondrial changes / C. Hegedus, G. Boros, E. A., Janka, E. Fidrus, T. Juhász, K. Karikó, G. Emri, P. Bai, É. Remenyik
Dátum:2019
ISSN:0022-202X 1523-1747
Tárgyszavak:Orvostudományok Elméleti orvostudományok poszter
folyóiratcikk
Megjelenés:Journal of Investigative Dermatology. - 139 : 9 (2019), p. S309. -
További szerzők:Boros Gábor (1980-) (biokémikus, molekuláris biológus) Janka Eszter Anna (1989-) (bőrgyógyász, népegészségügyi szakember) Fidrus Eszter (1992-) (biotechnológus) Juhász Tamás (1976-) (biológus, orvosbiológus) Karikó Katalin (1955-) (biológus, biokémikus) Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Bai Péter (1976-) (biokémikus) Remenyik Éva (1956-) (bőrgyógyász)
Pályázati támogatás:K120206
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM086261
035-os BibID:(WOS)000410115800622
Első szerző:Péter M.
Cím:Time-dependent investigation of UVB-induced cellular mechanisms in human keratinocytes using mRNA encoding cyclobutane pyrimidine dimer-specific photolyase / M. Péter, G. Boros, C. Hegedüs, E. Fidrus, G. Emri, K. Karikó, É. Remenyik
Dátum:2017
ISSN:0022-202X 1523-1747
Megjegyzések:In vitro-synthesized mRNA containing nucleotide modifications has distinguished therapeutic potential to transiently express physiologically important proteins. One such protein is photolyase, which accelerates the removal of UV-induced DNA damages, including cyclobutane pyrimidine dimers (CPD) using the energy of visible light (photoreactivation). Photolyase however is absent in humans. In our previous work, mRNA encoding CPD-specific photolyase has been effectively transfected into HaCaT cells. The encoded protein was visualized in the nuclei. Using CPD-specific ELISA, we showed that CPD-photolyase removed 90% of CPDs in the mRNA transfected cells at one hour after photoreactivation. Here, we found that the mechanism of DNA repair by CPD-photolyase shows a time-dependent behavior. To determine cell viability and apoptosis in photolyase mRNA transfected HaCaT keratinocytes flow cytometry was used. First, cells were exposed to UVB irradiation (20 mJ/cm2), and then photolyase was activated by photoreactivation at 6 h, 12 h and 24 h after UVB exposure. Photoreactivation performed at 6 h or 12 h after UVB irradiation the viability of cells was significantly higher compared to those kept in dark. However, no difference could be observed between the groups when the photoreactivation was delivered at 24 h after UVB irradiation, thus resulting significant keratinocytes death by apoptosis. These findings contribute to better understanding of UVB-induced cellular processes and give an opportunity for developing potential therapeutic agents which is effective not only before but even after UVB irradiation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok poszter
folyóiratcikk
Megjelenés:Journal of Investigative Dermatology. - 137 : 10 (2017), p. S301. -
További szerzők:Boros G. Hegedűs Csaba (1988-) (molekuláris biológus) Fidrus Eszter (1992-) (biotechnológus) Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Karikó Katalin (1955-) (biológus, biokémikus) Remenyik Éva (1956-) (bőrgyógyász)
Pályázati támogatás:GINOP-2.3.2-15-2016-00005
GINOP
K120206
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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