Quantitative Proteomic Profiling of Prematurely Senescent ARPE-19 Cells

Published

January 1, 2001

Author(s)

Illarion Turko, Wei-Li Liao

Abstract

Senescence of retinal pigment epithelial (RPE) cells is a crucial event in the pathogenesis of age-related macular degeneration (AMD). ARPE-19 is a nontransformed human RPE cell line that displays many differentiated properties typical of RPE in vivo. The study was designed to determine whether the protein profiles of control and prematurely senescent ARPE-19 cells exhibit differences and to identify differentially expressed proteins. Methods. Premature senescence of human ARPE-19 cells was induced by repeated treatments with 6 mM tert-butylhydroperoxide (tert-BHP). The relative quantification of selected proteins in the senescent cells versus control ARPE-19 cells was achieved by calculating the ratio of signal intensities for the deuterated and normal forms of cysteine-containing labeled peptides in MALDI-MS spectra. Results. Relative levels of 115 proteins were accessed. The changes in expression were found for 8 proteins. i) The upregulation of superoxide dismutases, cathepsin D, UCH-L1, and aldose reductase is most likely a typical defensive response to the oxidative stress and can be seen as beneficial. However, cathepsin D, UCH-L1, and aldose reductase have more than one activities and their upregulation could be a "double-edged sword" with potentially harmful consequences as well. ii) The downregulation of ribosomal proteins is most likely a typical secondary feature of senescent cells with growth cell arrest while the stress-induced downregulation of Ran could be a causal factor in growth cell arrest and therefore in senescence itself.

Citation

Investigative Ophthalmology & Visual Science

Pub Type

Journals

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Citation

Turko, I. and Liao, W. (2001), Quantitative Proteomic Profiling of Prematurely Senescent ARPE-19 Cells, Investigative Ophthalmology & Visual Science, [online], https://tsapps.nist.gov/publication/get_pdf.cfm?pub_id=903608 (Accessed April 27, 2024)