Aqueous humor-borne factor upregulates Bcl-2 expression in corneal endothelial cells

Xiao Yan Li, Brendan M. De Marco, Elizabeth S. Mayhew, Jerry Y. Niederkorn

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Purpose. To determine if factors present in the aqueous humor (AH) protect the corneal endothelium from apoptosis. Methods. Mouse and human corneal endothelial cells were cultured in vitro, and apoptosis was induced by nutrient deprivation. AH and supernatant from iris/ciliary body (I/CB) cell cultures were tested for their effect on corneal endothelial cell apoptosis. The effect of I/CB supernatant on Fas, Bax, and Bcl-2 gene transcription was evaluated by Northern blotting. I/CB supernatant was subjected to proteinase analysis to identify the apoptosis inhibitory factor(s). Results. Rabbit AH and supernatant from mouse I/CB cell cultures inhibited the apoptosis of mouse and human immortalized corneal endothelial cell lines. The inhibition of apoptosis was associated with an upregulation of Bcl-2 gene transcription and Bcl-2 protein expression. Bax gene expression was not significantly affected by I/CB cell supernatant. Induction of apoptosis by stimulation of the Fas receptor was unaffected by I/CB cell supernatant. Protease analyses indicated that the apoptosis inhibitory factor was a protein. Conclusions. The inability of corneal endothelial cells to undergo mitosis renders the corneal endothelium vulnerable to loss of physiological function through cellular attrition. However, a protein(s) produced by I/CB cells and present in the AH, upregulates Bcl-2 gene transcription and protects the corneal endothelial cells from apoptosis.

Original languageEnglish (US)
Pages (from-to)970-978
Number of pages9
JournalCurrent Eye Research
Volume17
Issue number10
DOIs
StatePublished - 1998

Fingerprint

Aqueous Humor
Ciliary Body
Iris
Up-Regulation
Endothelial Cells
Apoptosis
bcl-2 Genes
Corneal Endothelium
Peptide Hydrolases
Cell Culture Techniques
CD95 Antigens
Proteins
Mitosis
Northern Blotting
Rabbits
Gene Expression
Cell Line
Food

Keywords

  • Apoptosis
  • Aqueous humor
  • Bax
  • Bcl-2
  • Corneal endothelial cells
  • Human
  • Mouse

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Aqueous humor-borne factor upregulates Bcl-2 expression in corneal endothelial cells. / Li, Xiao Yan; De Marco, Brendan M.; Mayhew, Elizabeth S.; Niederkorn, Jerry Y.

In: Current Eye Research, Vol. 17, No. 10, 1998, p. 970-978.

Research output: Contribution to journalArticle

Li, Xiao Yan ; De Marco, Brendan M. ; Mayhew, Elizabeth S. ; Niederkorn, Jerry Y. / Aqueous humor-borne factor upregulates Bcl-2 expression in corneal endothelial cells. In: Current Eye Research. 1998 ; Vol. 17, No. 10. pp. 970-978.
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Y1 - 1998

N2 - Purpose. To determine if factors present in the aqueous humor (AH) protect the corneal endothelium from apoptosis. Methods. Mouse and human corneal endothelial cells were cultured in vitro, and apoptosis was induced by nutrient deprivation. AH and supernatant from iris/ciliary body (I/CB) cell cultures were tested for their effect on corneal endothelial cell apoptosis. The effect of I/CB supernatant on Fas, Bax, and Bcl-2 gene transcription was evaluated by Northern blotting. I/CB supernatant was subjected to proteinase analysis to identify the apoptosis inhibitory factor(s). Results. Rabbit AH and supernatant from mouse I/CB cell cultures inhibited the apoptosis of mouse and human immortalized corneal endothelial cell lines. The inhibition of apoptosis was associated with an upregulation of Bcl-2 gene transcription and Bcl-2 protein expression. Bax gene expression was not significantly affected by I/CB cell supernatant. Induction of apoptosis by stimulation of the Fas receptor was unaffected by I/CB cell supernatant. Protease analyses indicated that the apoptosis inhibitory factor was a protein. Conclusions. The inability of corneal endothelial cells to undergo mitosis renders the corneal endothelium vulnerable to loss of physiological function through cellular attrition. However, a protein(s) produced by I/CB cells and present in the AH, upregulates Bcl-2 gene transcription and protects the corneal endothelial cells from apoptosis.

AB - Purpose. To determine if factors present in the aqueous humor (AH) protect the corneal endothelium from apoptosis. Methods. Mouse and human corneal endothelial cells were cultured in vitro, and apoptosis was induced by nutrient deprivation. AH and supernatant from iris/ciliary body (I/CB) cell cultures were tested for their effect on corneal endothelial cell apoptosis. The effect of I/CB supernatant on Fas, Bax, and Bcl-2 gene transcription was evaluated by Northern blotting. I/CB supernatant was subjected to proteinase analysis to identify the apoptosis inhibitory factor(s). Results. Rabbit AH and supernatant from mouse I/CB cell cultures inhibited the apoptosis of mouse and human immortalized corneal endothelial cell lines. The inhibition of apoptosis was associated with an upregulation of Bcl-2 gene transcription and Bcl-2 protein expression. Bax gene expression was not significantly affected by I/CB cell supernatant. Induction of apoptosis by stimulation of the Fas receptor was unaffected by I/CB cell supernatant. Protease analyses indicated that the apoptosis inhibitory factor was a protein. Conclusions. The inability of corneal endothelial cells to undergo mitosis renders the corneal endothelium vulnerable to loss of physiological function through cellular attrition. However, a protein(s) produced by I/CB cells and present in the AH, upregulates Bcl-2 gene transcription and protects the corneal endothelial cells from apoptosis.

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KW - Corneal endothelial cells

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KW - Mouse

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