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Tedja, M.S.* ; Wojciechowski, R.* ; Hysi, P.G.* ; Eriksson, N.* ; Furlotte, N.A.* ; Verhoeven, V.J.M.* ; Iglesias, A.I.* ; Meester-Smoor, M.A.* ; Tompson, S.W.* ; Fan, Q.* ; Khawaja, A.P.* ; Cheng, C.Y.* ; Höhn, R.* ; Yamashiro, K.* ; Wenocur, A.* ; Grazal, C.* ; Haller, T.* ; Metspalu, A.* ; Wedenoja, J.* ; Jonas, J.B.* ; Wang, Y.X.* ; Xie, J.* ; Mitchell, P.* ; Foster, P.J.* ; Klein, B.E.K.* ; Klein, R.* ; Paterson, A.D.* ; Hosseini, S.M.* ; Shah, R.L.* ; Williams, C.* ; Teo, Y.Y.* ; Tham, Y.C.* ; Gupta, P.* ; Zhao, W.* ; Shi, Y.* ; Saw, W.Y.* ; Tai, E.S.* ; Sim, X.L.* ; Huffman, J.E.* ; Polašek, O.* ; Hayward, C.* ; Bencic, G.* ; Rudan, I.* ; Wilson, J.F.* ; Joshi, P.K.* ; Tsujikawa, A.* ; Matsuda, F.* ; Whisenhunt, K.N.* ; Zeller, T.* ; van der Spek, P.J.* ; Haak, R.* ; Meijers-Heijboer, H.* ; van Leeuwen, E.M.* ; Iyengar, S.K.* ; Lass, J.H.* ; Hofman, A.* ; Rivadeneira, F.* ; Uitterlinden, A.G.* ; Vingerling, J.R.* ; Lehtimäki, T.* ; Raitakari, O.T.* ; Biino, G.* ; Concas, M.P.* ; Schwantes-An, T.H.* ; Igo, R.P.* ; Cuellar-Partida, G.* ; Martin, N.G.* ; Craig, J.E.* ; Gharahkhani, P.* ; Williams, K.M.* ; Nag, A.* ; Rahi, J.S.* ; Cumberland, P.M.* ; Delcourt, C.* ; Bellenguez, C.* ; Ried, J.S. ; Bergen, A.A.* ; Meitinger, T. ; Gieger, C. ; Wong, T.Y.* ; Hewitt, A.W.* ; Mackey, D.A.* ; Simpson, C.L.* ; Pfeiffer, N.* ; Pärssinen, O.* ; Baird, P.N.* ; Vitart, V.* ; Amin, N.* ; van Duijn, C.M.* ; Bailey-Wilson, J.E.* ; Young, T.L.* ; Saw, S.M.* ; Stambolian, D.* ; MacGregor, S.* ; Guggenheim, J.A.* ; Tung, J.Y.* ; Hammond, C.J.* ; Klaver, C.C.W.*

Genome-wide association meta-analysis highlights light-induced signaling as a driver for refractive error.

Nat. Genet. 50, 834-848 (2018)
Postprint DOI PMC
Open Access Green
Skin affections after sulfur mustard (SM) exposure include erythema, blister formation and severe inflammation. An antidote or specific therapy does not exist. Anti-inflammatory compounds as well as substances counteracting SM-induced cell death are under investigation. In this study, we investigated the benzylisoquinoline alkaloide berberine (BER), a metabolite in plants like berberis vulgaris, which is used as herbal pharmaceutical in Asian countries, against SM toxicity using a well-established in vitro approach. Keratinocyte (HaCaT) mono-cultures (MoC) or HaCaT/THP-1 co-cultures (CoC) were challenged with 100, 200 or 300 mM SM for 1 h. Post-exposure, both MoC and CoC were treated with 10, 30 or 50 mu M BER for 24 h. At that time, supernatants were collected and analyzed both for interleukine (IL) 6 and 8 levels and for content of adenylate-kinase (AK) as surrogate marker for cell necrosis. Cells were lysed and nucleosome formation as marker for late apoptosis was assessed. In parallel, AK in cells was determined for normalization purposes. BER treatment did not influence necrosis, but significantly decreased apoptosis. Anti-inflammatory effects were moderate, but also significant, primarily in CoC. Overall, BER has protective effects against SM toxicity in vitro. Whether this holds true should be evaluated in future in vivo studies.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Cell-line Thp-1; In-vitro; Hacat Keratinocytes; Alkaloid Berberine; Dendritic Cells; Injury; Skin; Sensitization; Expression; Toxicity
ISSN (print) / ISBN 1061-4036
e-ISSN 1546-1718
Zeitschrift Nature Genetics
Quellenangaben Band: 50, Heft: 6, Seiten: 834-848 Artikelnummer: , Supplement: ,
Verlag Nature Publishing Group
Verlagsort New York, NY
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Genetic Epidemiology (IGE)
Institute of Human Genetics (IHG)
Institute of Epidemiology II (EPI2)