Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway
Abstract
Highlights: Black-Right-Pointing-Pointer UVB radiated skin keratinocytes show cyclophilin D (Cyp-D) upregulation. Black-Right-Pointing-Pointer NAC inhibits UVB induced Cyp-D expression, while H{sub 2}O{sub 2} facilitates it. Black-Right-Pointing-Pointer Cyp-D-deficient cells are significantly less susceptible to UVB induced cell death. Black-Right-Pointing-Pointer Over-expression of Cyp-D causes spontaneous keratinocytes cell death. -- Abstract: UVB-induced skin cell damage involves the opening of mitochondrial permeability transition pore (mPTP), which leads to both apoptotic and necrotic cell death. Cyclophilin D (Cyp-D) translocation to the inner membrane of mitochondrion acts as a key component to open the mPTP. Our Western-Blot results in primary cultured human skin keratinocytes and in HaCaT cell line demonstrated that UVB radiation and hydrogen peroxide (H{sub 2}O{sub 2}) induced Cyp-D expression, which was inhibited by anti-oxidant N-acetyl cysteine (NAC). We created a stable Cyp-D deficiency skin keratinocytes by expressing Cyp-D-shRNA through lentiviral infection. Cyp-D-deficient cells were significantly less susceptible than their counterparts to UVB- or H{sub 2}O{sub 2}-induced cell death. Further, cyclosporine A (Cs-A), a Cyp-D inhibitor, inhibited UVB- or H{sub 2}O{sub 2}-induced keratinocytes cell death. Reversely, over-expression of Cyp-D in primary keratinocytes caused spontaneous keratinocytes cell death. These results suggest Cyp-D's critical role in UVB/oxidative stress-induced skin cell death.
- Authors:
-
- Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210024, Jiangsu (China)
- Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040 (China)
- Department of Dermatology, The First Affiliated Hospital of Kunming Medical University, Yunnan Provincial Institute of Dermatology, Kunming 650032, Yunnan (China)
- Department of Otorhinolaryngology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210024, Jiangsu (China)
- Department of Dermatology, BenQ Medical Center, Nanjing Medical University, Nanjing 210019, Jiangsu (China)
- Publication Date:
- OSTI Identifier:
- 22210232
- Resource Type:
- Journal Article
- Journal Name:
- Biochemical and Biophysical Research Communications
- Additional Journal Information:
- Journal Volume: 425; Journal Issue: 4; Other Information: Copyright (c) 2012 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 60 APPLIED LIFE SCIENCES; APOPTOSIS; CYCLOSPORINE; CYSTEINE; HYDROGEN PEROXIDE; MITOCHONDRIA; OXIDATION; OXIDIZERS; OXYGEN; PERMEABILITY; SKIN; TRANSLOCATION; ULTRAVIOLET RADIATION
Citation Formats
Ji, Chao, Yang, Bo, Yang, Zhi, Tu, Ying, Yang, Yan-li, He, Li, and Bi, Zhi-Gang. Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway. United States: N. p., 2012.
Web. doi:10.1016/J.BBRC.2012.07.160.
Ji, Chao, Yang, Bo, Yang, Zhi, Tu, Ying, Yang, Yan-li, He, Li, & Bi, Zhi-Gang. Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway. United States. https://doi.org/10.1016/J.BBRC.2012.07.160
Ji, Chao, Yang, Bo, Yang, Zhi, Tu, Ying, Yang, Yan-li, He, Li, and Bi, Zhi-Gang. 2012.
"Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway". United States. https://doi.org/10.1016/J.BBRC.2012.07.160.
@article{osti_22210232,
title = {Ultra-violet B (UVB)-induced skin cell death occurs through a cyclophilin D intrinsic signaling pathway},
author = {Ji, Chao and Yang, Bo and Yang, Zhi and Tu, Ying and Yang, Yan-li and He, Li and Bi, Zhi-Gang},
abstractNote = {Highlights: Black-Right-Pointing-Pointer UVB radiated skin keratinocytes show cyclophilin D (Cyp-D) upregulation. Black-Right-Pointing-Pointer NAC inhibits UVB induced Cyp-D expression, while H{sub 2}O{sub 2} facilitates it. Black-Right-Pointing-Pointer Cyp-D-deficient cells are significantly less susceptible to UVB induced cell death. Black-Right-Pointing-Pointer Over-expression of Cyp-D causes spontaneous keratinocytes cell death. -- Abstract: UVB-induced skin cell damage involves the opening of mitochondrial permeability transition pore (mPTP), which leads to both apoptotic and necrotic cell death. Cyclophilin D (Cyp-D) translocation to the inner membrane of mitochondrion acts as a key component to open the mPTP. Our Western-Blot results in primary cultured human skin keratinocytes and in HaCaT cell line demonstrated that UVB radiation and hydrogen peroxide (H{sub 2}O{sub 2}) induced Cyp-D expression, which was inhibited by anti-oxidant N-acetyl cysteine (NAC). We created a stable Cyp-D deficiency skin keratinocytes by expressing Cyp-D-shRNA through lentiviral infection. Cyp-D-deficient cells were significantly less susceptible than their counterparts to UVB- or H{sub 2}O{sub 2}-induced cell death. Further, cyclosporine A (Cs-A), a Cyp-D inhibitor, inhibited UVB- or H{sub 2}O{sub 2}-induced keratinocytes cell death. Reversely, over-expression of Cyp-D in primary keratinocytes caused spontaneous keratinocytes cell death. These results suggest Cyp-D's critical role in UVB/oxidative stress-induced skin cell death.},
doi = {10.1016/J.BBRC.2012.07.160},
url = {https://www.osti.gov/biblio/22210232},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 4,
volume = 425,
place = {United States},
year = {Fri Sep 07 00:00:00 EDT 2012},
month = {Fri Sep 07 00:00:00 EDT 2012}
}