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PTEN Reduced UVB-Mediated Apoptosis in Retinal Pigment Epithelium Cells.

Abstract Age-related macular degeneration (AMD) is a leading cause of blindness and progressive loss of central vision in the elderly population. The important factor of AMD pathogenesis is the degeneration of retinal pigment epithelial (RPE) cells by oxidative stress. Inactivation of PTEN can disrupt intercellular adhesion in the RPE cells, but the mechanism of oxidative stress is less known. Here we presented evidence that UVB-mediated oxidative stress induced apoptosis in ARPE-19 cells. Downregulation of the expression of PTEN in UVB-irradiative RPE cells triggered DNA damage and increased the level of UVB-induced apoptosis by activating p53-dependent pathway. However, overexpression of PTEN increased cell survival by suppressing p-H2A in response to DNA damage and apoptosis. When using Pifithrin-α (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis. Thus, it elucidated the molecular mechanisms of UVB-induced damage in RPE cells and may offer an alternative therapeutic target in dry AMD.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28321407
OWN - NLM
STAT- MEDLINE
DA  - 20170321
DCOM- 20170322
LR  - 20170322
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - PTEN Reduced UVB-Mediated Apoptosis in Retinal Pigment Epithelium Cells.
PG  - 3681707
LID - 10.1155/2017/3681707 [doi]
AB  - Age-related macular degeneration (AMD) is a leading cause of blindness and
      progressive loss of central vision in the elderly population. The important
      factor of AMD pathogenesis is the degeneration of retinal pigment epithelial
      (RPE) cells by oxidative stress. Inactivation of PTEN can disrupt intercellular
      adhesion in the RPE cells, but the mechanism of oxidative stress is less known.
      Here we presented evidence that UVB-mediated oxidative stress induced apoptosis
      in ARPE-19 cells. Downregulation of the expression of PTEN in UVB-irradiative RPE
      cells triggered DNA damage and increased the level of UVB-induced apoptosis by
      activating p53-dependent pathway. However, overexpression of PTEN increased cell 
      survival by suppressing p-H2A in response to DNA damage and apoptosis. When using
      Pifithrin-alpha (one of p53 inhibitors), the level of p53-dependent apoptosis was
      significantly lower than untreated, which suggested that p53 was possibly
      involved in PTEN-dependent apoptosis. Thus, it elucidated the molecular
      mechanisms of UVB-induced damage in RPE cells and may offer an alternative
      therapeutic target in dry AMD.
FAU - He, Jia
AU  - He J
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Long, Chongde
AU  - Long C
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Huang, Zixin
AU  - Huang Z
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Zhou, Xin
AU  - Zhou X
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Kuang, Xielan
AU  - Kuang X
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China; Biobank of Eye, State Key
      Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University,
      54 Xianlie Road, Guangzhou 510060, China.
FAU - Liu, Lanying
AU  - Liu L
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Liu, Huijun
AU  - Liu H
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Tang, Yan
AU  - Tang Y
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Fan, Yuting
AU  - Fan Y
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Ning, Jie
AU  - Ning J
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Ma, Xinqi
AU  - Ma X
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Zhang, Qingjiong
AU  - Zhang Q
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China.
FAU - Shen, Huangxuan
AU  - Shen H
AUID- ORCID: 0000-0002-6552-9541
AD  - State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen
      University, 54 Xianlie Road, Guangzhou 510060, China; Biobank of Eye, State Key
      Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University,
      54 Xianlie Road, Guangzhou 510060, China.
LA  - eng
PT  - Journal Article
DEP - 20170222
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (Benzothiazoles)
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 3FPU23BG52 (Toluene)
RN  - D213B92S1Y (pifithrin)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (PTEN protein, human)
SB  - IM
MH  - Apoptosis/drug effects/*radiation effects
MH  - Benzothiazoles/pharmacology
MH  - Cell Line
MH  - Cell Survival/drug effects/radiation effects
MH  - Down-Regulation/drug effects/radiation effects
MH  - Gene Expression Regulation, Enzymologic/drug effects/radiation effects
MH  - Humans
MH  - Macular Degeneration/*enzymology/pathology
MH  - Oxidative Stress/drug effects/*radiation effects
MH  - PTEN Phosphohydrolase/*biosynthesis
MH  - Retinal Pigment Epithelium/*enzymology/pathology
MH  - Toluene/analogs & derivatives/pharmacology
MH  - Tumor Suppressor Protein p53/antagonists & inhibitors/metabolism
MH  - Ultraviolet Rays/*adverse effects
PMC - PMC5340936
COI - The authors declare that there is no conflict of interests regarding the
      publication of this paper.
EDAT- 2017/03/23 06:00
MHDA- 2017/03/23 06:01
CRDT- 2017/03/22 06:00
PHST- 2016/10/26 [received]
PHST- 2017/01/22 [revised]
PHST- 2017/01/26 [accepted]
AID - 10.1155/2017/3681707 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:3681707. doi: 10.1155/2017/3681707. Epub 2017 Feb 22.

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