Mitochondrial decay and impairment of antioxidant defenses in aging RPE cells

Research output: Chapter in Book/Report/Conference proceedingConference contribution

25 Scopus citations

Abstract

In the eye, the retinal pigment epithelium (RPE) is exposed to a highly oxidative environment, partly due to elevated oxygen partial pressure from the choriocapillaris and to digestion of polyunsaturated fatty acid laden photoreceptor outer segments. Here we examined the vulnerability of RPE cells to stress and changes in their mitochondria with increased chronological aging and showed that there is greater sensitivity of the cells to oxidative stress, alterations in their mitochondrial number, size, shape, matrix density, cristae architecture, and membrane integrity as a function of age. These features correlate with reduced cellular levels of ATP, ROS, and [Ca2+] c, lower Δψm, increased [Ca2+]m sequestration and decreased expression of mtHsp70, UCP2, and SOD3. Mitochondrial decay, bioenergetic deficiencies, and weakened antioxidant defenses in RPE cells occur as early as age 62. With increased severity, these conditions may significantly reduce RPE function in the retina and contribute to age related retinal anomalies.

Original languageEnglish (US)
Title of host publicationRetinal Degenerative Diseases
Subtitle of host publicationLaboratory and Therapeutic Investigations
EditorsRobert Anderson, Nawajes Mandal, Joe Hollyfield, Matthew LaVail
Pages165-183
Number of pages19
DOIs
StatePublished - Dec 1 2010

Publication series

NameAdvances in Experimental Medicine and Biology
Volume664
ISSN (Print)0065-2598

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)

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    He, Y., & Tombran-Tink, J. (2010). Mitochondrial decay and impairment of antioxidant defenses in aging RPE cells. In R. Anderson, N. Mandal, J. Hollyfield, & M. LaVail (Eds.), Retinal Degenerative Diseases: Laboratory and Therapeutic Investigations (pp. 165-183). (Advances in Experimental Medicine and Biology; Vol. 664). https://doi.org/10.1007/978-1-4419-1399-9_20