UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis

Narrow band (311 nm) UVB phototherapy is established treatment for psoriasis. DNA is a target for UVB via formation of cyclobutane pyrimidine dimers, which trigger loss of dendritic cells and macrophages, and inhibit CD4+ and CD8+ T cells. UV causes the formation of thymine dimers, which activate nu...

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Main Authors: Małgorzata Bernacka, Agata Liszewska, Ewa Robak, Anna Woźniacka, Jarosław Bogaczewicz
Format: Article
Language:English
Published: Termedia Publishing House 2019-01-01
Series:Przegląd Dermatologiczny
Subjects:
Online Access:https://www.termedia.pl/UVB-311-nm-phototherapy-and-NAD-NADH-metabolism-in-keratinocytes-in-patients-with-psoriasis,56,34454,1,1.html
id doaj-3330c58b1f514bc8b087ad0cce00da82
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spelling doaj-3330c58b1f514bc8b087ad0cce00da822020-11-25T00:02:42ZengTermedia Publishing HousePrzegląd Dermatologiczny0033-25262084-98932019-01-01105671071510.5114/dr.2018.8083934454UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasisMałgorzata BernackaAgata LiszewskaEwa RobakAnna WoźniackaJarosław BogaczewiczNarrow band (311 nm) UVB phototherapy is established treatment for psoriasis. DNA is a target for UVB via formation of cyclobutane pyrimidine dimers, which trigger loss of dendritic cells and macrophages, and inhibit CD4+ and CD8+ T cells. UV causes the formation of thymine dimers, which activate nuclear enzyme poly(ADP-ribose) polymerase. The fact that poly(ADP-ribose) polymerase utilizes nicotinamide-adenine dinucleotide (NAD) explains NAD decreases after UV irradiation. NADH regulates transcriptional repressor carboxyl-terminal binding protein, whereas NAD(+) is a co-substrate in deacylation reactions, engaged in genomic silencing. Hyperproliferation of psoriatic keratinocytes requires NADH during oxidative phosphorylation. In one study the NADH fluorescence (reflecting NADH amount) was reduced in psoriatic lesions. NAD(+) used topically was as effective as 0.1% anthralin. Spectrophotometry enables real-time measurements of NADH fluorescence in vivo in the epidermis and points out a new direction for application of biophysics in medicine.https://www.termedia.pl/UVB-311-nm-phototherapy-and-NAD-NADH-metabolism-in-keratinocytes-in-patients-with-psoriasis,56,34454,1,1.htmlultraviolet psoriasis nicotinamide-adenine dinucleotide spectrophotometry
collection DOAJ
language English
format Article
sources DOAJ
author Małgorzata Bernacka
Agata Liszewska
Ewa Robak
Anna Woźniacka
Jarosław Bogaczewicz
spellingShingle Małgorzata Bernacka
Agata Liszewska
Ewa Robak
Anna Woźniacka
Jarosław Bogaczewicz
UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
Przegląd Dermatologiczny
ultraviolet
psoriasis
nicotinamide-adenine dinucleotide
spectrophotometry
author_facet Małgorzata Bernacka
Agata Liszewska
Ewa Robak
Anna Woźniacka
Jarosław Bogaczewicz
author_sort Małgorzata Bernacka
title UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
title_short UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
title_full UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
title_fullStr UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
title_full_unstemmed UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis
title_sort uvb-311 nm phototherapy and nad(+)/nadh metabolism in keratinocytes in patients with psoriasis
publisher Termedia Publishing House
series Przegląd Dermatologiczny
issn 0033-2526
2084-9893
publishDate 2019-01-01
description Narrow band (311 nm) UVB phototherapy is established treatment for psoriasis. DNA is a target for UVB via formation of cyclobutane pyrimidine dimers, which trigger loss of dendritic cells and macrophages, and inhibit CD4+ and CD8+ T cells. UV causes the formation of thymine dimers, which activate nuclear enzyme poly(ADP-ribose) polymerase. The fact that poly(ADP-ribose) polymerase utilizes nicotinamide-adenine dinucleotide (NAD) explains NAD decreases after UV irradiation. NADH regulates transcriptional repressor carboxyl-terminal binding protein, whereas NAD(+) is a co-substrate in deacylation reactions, engaged in genomic silencing. Hyperproliferation of psoriatic keratinocytes requires NADH during oxidative phosphorylation. In one study the NADH fluorescence (reflecting NADH amount) was reduced in psoriatic lesions. NAD(+) used topically was as effective as 0.1% anthralin. Spectrophotometry enables real-time measurements of NADH fluorescence in vivo in the epidermis and points out a new direction for application of biophysics in medicine.
topic ultraviolet
psoriasis
nicotinamide-adenine dinucleotide
spectrophotometry
url https://www.termedia.pl/UVB-311-nm-phototherapy-and-NAD-NADH-metabolism-in-keratinocytes-in-patients-with-psoriasis,56,34454,1,1.html
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