Microarray analysis of H2O2-, HNE-, or tBH-treated ARPE-19 cells
- PMID: 12419474
- DOI: 10.1016/s0891-5849(02)01082-1
Microarray analysis of H2O2-, HNE-, or tBH-treated ARPE-19 cells
Abstract
Oxidative stress plays a key role in aging diseases of the posterior pole of the eye such as age-related macular degeneration. The oxidative stress response of in vitro RPE cells has been studied for a small number of genes. However, a comprehensive transcriptional response has yet to be elucidated. The purpose of this study was to determine if the transcription of a common set of genes is altered by exposure of ARPE-19 cells to three major generators of oxidative stress, hydrogen peroxide (H2O2), 4-hydroxynonenal (HNE), and tert-butylhydroperoxide (tBH). As expected, a common response was observed that included 35 genes differentially regulated by all three treatments. Of these, only one gene was upregulated, and only by one oxidant, while all other responses were downregulation. The majority of these genes fell into five functional categories: apoptosis, cell cycle regulation, cell-cell communication, signal transduction, and transcriptional regulation. Additionally, a large number of genes were differentially regulated by one oxidant only, including the majority of the conventional oxidative stress response genes present on the Clontech Human 1.2 microarray. This study raises questions regarding the generality of results that involve the use of a single oxidant and a single cell culture condition.
Similar articles
-
Differential effects of PPARgamma ligands on oxidative stress-induced death of retinal pigmented epithelial cells.Invest Ophthalmol Vis Sci. 2011 Feb 22;52(2):890-903. doi: 10.1167/iovs.10-5715. Invest Ophthalmol Vis Sci. 2011. PMID: 20847119
-
Downregulation of differentiation specific gene expression by oxidative stress in ARPE-19 cells.Invest Ophthalmol Vis Sci. 2001 Oct;42(11):2706-13. Invest Ophthalmol Vis Sci. 2001. PMID: 11581219
-
Stimulation of apical and basolateral VEGF-A and VEGF-C secretion by oxidative stress in polarized retinal pigment epithelial cells.Mol Vis. 2006 Dec 22;12:1649-59. Mol Vis. 2006. PMID: 17200665
-
Endoplasmic reticulum stress induced by oxidative stress in retinal pigment epithelial cells.Graefes Arch Clin Exp Ophthalmol. 2008 May;246(5):677-83. doi: 10.1007/s00417-008-0770-2. Epub 2008 Feb 16. Graefes Arch Clin Exp Ophthalmol. 2008. PMID: 18278507
-
Density-dependent expression of FGF-2 in response to oxidative stress in RPE cells in vitro.Curr Eye Res. 2001 Sep;23(3):226-31. doi: 10.1076/ceyr.23.3.226.5467. Curr Eye Res. 2001. PMID: 11803485
Cited by
-
Oxidative stress, bone marrow failure, and genome instability in hematopoietic stem cells.Int J Mol Sci. 2015 Jan 22;16(2):2366-85. doi: 10.3390/ijms16022366. Int J Mol Sci. 2015. PMID: 25622253 Free PMC article. Review.
-
The p53 tumor suppressor network is a key responder to microenvironmental components of chronic inflammatory stress.Cancer Res. 2005 Nov 15;65(22):10255-64. doi: 10.1158/0008-5472.CAN-05-1714. Cancer Res. 2005. PMID: 16288013 Free PMC article.
-
BMP4 mediates oxidative stress-induced retinal pigment epithelial cell senescence and is overexpressed in age-related macular degeneration.J Biol Chem. 2009 Apr 3;284(14):9529-39. doi: 10.1074/jbc.M809393200. Epub 2009 Jan 21. J Biol Chem. 2009. PMID: 19158083 Free PMC article.
-
TRANSCRIPTIONAL AND PHOSPHO-PROTEOMIC SCREENS REVEAL STEM CELL ACTIVATION OF INSULIN-RESISTANCE AND TRANSFORMATION PATHWAYS FOLLOWING A SINGLE MINIMALLY TOXIC EPISODE OF ROS.Int J Genomics Proteomics. 2011;2(1):34-49. Int J Genomics Proteomics. 2011. PMID: 21743783 Free PMC article.
-
Involvement of MicroRNAs in hydrogen peroxide-mediated gene regulation and cellular injury response in vascular smooth muscle cells.J Biol Chem. 2009 Mar 20;284(12):7903-13. doi: 10.1074/jbc.M806920200. Epub 2009 Jan 21. J Biol Chem. 2009. PMID: 19158092 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Research Materials
