Document Detail

Up-regulation of NDRG2 in senescent lens epithelial cells contributes to age-related cataract in human.
MedLine Citation:
PMID:  22043305     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Human N-Myc downstream regulated gene2 (NDRG2), a novel gene has been cloned and shown to be related to a number of cellular processes, including proliferation, differentiation, stress, and apoptosis. NDRG2 has also been linked to age-related Alzheimer's disease. Since the role of this gene in senescence is limited, we have investigated the potential role of NDRG2 in human lens epithelial cells (HLECs), a paradigm implicated in age-related cataract.
METHODOLOGY/PRINCIPAL FINDINGS: Cultured HLECs (SRA01/04) were subjected to prolonged exposure to low dose of H(2)O(2) to simulate senescence. After being exposed to 50 µM H(2)O(2) for 2 weeks, HLECs senescent-morphological changes appeared, cell viability decreased dramatically, cell proliferation reduced from 37.4% to 16.1%, and senescence-associated β-galactosidase activity increased from 0 to 90.3%. Ndrg2 protein expression was also significantly increased in these senescent cells. To induce overexpression of NDRG2, SRA01/04 cells were infected with the adenoviral vector of NDRG2. In these cells, overexpression of NDRG2 resulted in a fibroblast-like appearance and the cell viability decreased about 20%. In addition, the NDRG2-overexpression cells demonstrated 20% lower viability when exposed to 50-200 µM H(2)O(2) for acute oxidative stress. Furthermore, the expression of NDRG2 from age-related cataracts was up-regulated 2-fold at both mRNA and protein levels compared with the clear lenses.
CONCLUSIONS/SIGNIFICANCE: NDRG2 is up regulated not only in the ageing process of HLECs in vitro but also in the cells from human age-related cortical cataract in vivo. Up-regulation of NDRG2 induces cell morphological changes, reduces cell viability, and especially lowers cellular resistance to oxidative stress. NDRG2-mediated affects in HLECs may associate with age-related cataract formation.
Zi-Feng Zhang; Jian Zhang; Yan-Nian Hui; Min-Hua Zheng; Xin-Ping Liu; Peter F Kador; Yu-Sheng Wang; Li-Bo Yao; Jian Zhou
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-10-17
Journal Detail:
Title:  PloS one     Volume:  6     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2011  
Date Detail:
Created Date:  2011-11-01     Completed Date:  2012-04-06     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e26102     Citation Subset:  IM    
Department of Ophthalmology, Eye Institute of Chinese PLA, Xi-Jing Hospital, Fourth Military Medical University, Xi'an, China.
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MeSH Terms
Cataract / etiology*
Cell Aging / drug effects*
Cell Proliferation
Cell Shape
Cell Survival
Cells, Cultured
Epithelial Cells / metabolism*
Hydrogen Peroxide / pharmacology
Lens, Crystalline / cytology*
Oxidative Stress
Tumor Suppressor Proteins / analysis,  physiology*
Reg. No./Substance:
0/NDRG2 protein, human; 0/Tumor Suppressor Proteins; 7722-84-1/Hydrogen Peroxide

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