May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
Smoke Induce Cellular Senescence and Cell Loss in Retinal Pigment Epithelium Cells
Author Affiliations & Notes
  • R. Alsaeidi
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • A. Yu
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • M. Kernt
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • J. Burger
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • A. Kampik
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • U. Welge-Lussen
    University Eye Hospital, Ludwig- Maximillian University, Munich, Germany
  • Footnotes
    Commercial Relationships R. Alsaeidi, None; A. Yu, None; M. Kernt, None; J. Burger, None; A. Kampik, None; U. Welge-Lussen, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 556. doi:
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    • Get Citation

      R. Alsaeidi, A. Yu, M. Kernt, J. Burger, A. Kampik, U. Welge-Lussen; Smoke Induce Cellular Senescence and Cell Loss in Retinal Pigment Epithelium Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):556.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose:: Age related macular degeneration (AMD) is the leading cause of blindness. This disease is characterized by loss of retinal pigment epithelium (RPE) cells and cellular senescence. Characteristically findings of cellular senescence are increased activity of beta galactosidase a elevated expression of senescence associated (SA) genes like ApoJ/clusterin, connective tissue growth factor (CTGF) and fibronectin (FN). Epidemiological studies have shown increased risk of AMD due to smoking. So far the smoke induced cellular events leading to AMD are not clear.

Methods:: Cultured RPE cells from 5 donors, passage 3-5 were exposed to cigarette smoke condensate (CSC) in a concentration (Co) from 2 - 12 % for 24 hours. After exposure cells were kept for 72 h under serum free conditions. Cellular senescence was investigated by expression of senescence associated beta- galactosidase staining. The age related genes ApoJ/clusterin, CTGF and FN were examined by real time PCR . Cell survival was investigated by MTT assay and life dead staining.

Results:: The proliferation of RPE cells was dose dependently inhibited by increasing CSC concentrations (2% CSC = 96% +/- 3,4; 4% = 92% +/- 7,2; 8% = 93% +/- 12,3; 12% = 46% +/- 9,8). The concentration of 12% of CSC induced marked cell death (12% = 88% +/- 12,4). Concentration of 2%; 4% and 8% of CSC induced the expression of ß-gal positive RPE cells (Co = 3,5 % +/- 0.6; 2% CSC = 12 % +/- 1.4; 4% CSC = 16 +/- 1.7; 8 % CSC = 92% +/- 17) and the expression of SA genes ApoJ/ clusterin (Co = 100: 2 % CSC = 115 +/- 15 ; 4 % CSC = 187 +/- 29; 8 % CSC = 288 +/- 26 ), CTGF (Co = 100: 2 % CSC = 283 +/- 35; 4% CSC = 533 +/- 43,9%; 8 % CSC = 975 +/- 57 ), and FN (Co = 100: 2 % CSC = 115 +/-15; 4 % CSC = 296 +/- 43; 8 % CSC = 743 % +/- 57).

Conclusions:: Our in vitro experiments clearly show a smoke induced loss and advanced senescence of RPE cells. Beside the recommendations to stop smoking targeting smoke induced cellular events could help to lower the incidence of AMD.

Keywords: apoptosis/cell death • ocular irritancy/toxicity testing • age-related macular degeneration 
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