A2E selectively induces COX-2 in ARPE-19 and human neural cells

Walter J. Lukiw, Pranab K. Mukherjee, Jian Guo Cui, Nicolas G. Bazan

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Purpose: To investigate the expression of cyclooxygenase (COX)-1, -2, and -3 RNA and protein in retinal pigment epithelial (ARPE-19) cells and in human neural (HN) cells exposed to the stress-inducing cytokines IL-1β and TNF-α, the oxidizing peroxide H2O2, the combination of TNF-α + H2O2, and the lipofuscin fluorophore A2E. Methods: Three-week-old ARPE-19 and HN cells were incubated with IL-1β (10 ng/ml), TNF-α (10 ng/ml), H2O2 (0.6 μM), TNF-α + H2O2 (10 ng/ml and 0.6 μM), or A2E (10 μM) for 8 hr, after which total RNA and whole cellular proteins were isolated. Cyclooxygenase-1, -2, and -3 RNA and protein levels were quantified using Northern and Western immunoassay. Results: IL-1β-, H 2O2-, TNF-α-, TNF-α + H2O 2-, or A2E-stressed ARPE-19 or HN cells displayed no significant up-regulation in COX-1 or COX-3 RNA message abundance; however, significant upregulation was observed in COX-2 RNA message and protein abundance. A2E treatment of HN cells resulted in modest increases in COX-3 protein, an effect that was not observed in ARPE-19 cells. Conclusions: COX-2 RNA levels were induced in cytokine-, peroxide-, and A2E-stressed ARPE-19 and HN cells. Lack of induction of COX-3 RNA message by A2E, coupled with increases in COX-3 protein under identical treatment conditions, suggest that significant post-transcriptional or post-translational controls may regulate COX-3 gene expression in HN cells. Stress-induced upregulation of COX-2 gene expression in ARPE-19 and HN cells may play a mechanistic role in promoting proinflammatory and/or pro-oxidative pathology in these tissues.

Original languageEnglish
Pages (from-to)259-263
Number of pages5
JournalCurrent Eye Research
Volume31
Issue number3
DOIs
StatePublished - Mar 1 2006

Fingerprint

Cyclooxygenase 2
RNA
Cyclooxygenase 1
Interleukin-1
Proteins
Up-Regulation
Peroxides
Cytokines
Gene Expression
Lipofuscin
Retinal Pigments
Immunoassay
Interleukin-10
cyclooxygenase-3
Pathology

Keywords

  • A2E
  • ARPE-19
  • COX-1
  • COX-2
  • COX-3
  • Cyclooxygenase
  • Human neural (HN) cells

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Lukiw, W. J., Mukherjee, P. K., Cui, J. G., & Bazan, N. G. (2006). A2E selectively induces COX-2 in ARPE-19 and human neural cells. Current Eye Research, 31(3), 259-263. https://doi.org/10.1080/02713680600556974

A2E selectively induces COX-2 in ARPE-19 and human neural cells. / Lukiw, Walter J.; Mukherjee, Pranab K.; Cui, Jian Guo; Bazan, Nicolas G.

In: Current Eye Research, Vol. 31, No. 3, 01.03.2006, p. 259-263.

Research output: Contribution to journalArticle

Lukiw, WJ, Mukherjee, PK, Cui, JG & Bazan, NG 2006, 'A2E selectively induces COX-2 in ARPE-19 and human neural cells', Current Eye Research, vol. 31, no. 3, pp. 259-263. https://doi.org/10.1080/02713680600556974
Lukiw, Walter J. ; Mukherjee, Pranab K. ; Cui, Jian Guo ; Bazan, Nicolas G. / A2E selectively induces COX-2 in ARPE-19 and human neural cells. In: Current Eye Research. 2006 ; Vol. 31, No. 3. pp. 259-263.
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abstract = "Purpose: To investigate the expression of cyclooxygenase (COX)-1, -2, and -3 RNA and protein in retinal pigment epithelial (ARPE-19) cells and in human neural (HN) cells exposed to the stress-inducing cytokines IL-1β and TNF-α, the oxidizing peroxide H2O2, the combination of TNF-α + H2O2, and the lipofuscin fluorophore A2E. Methods: Three-week-old ARPE-19 and HN cells were incubated with IL-1β (10 ng/ml), TNF-α (10 ng/ml), H2O2 (0.6 μM), TNF-α + H2O2 (10 ng/ml and 0.6 μM), or A2E (10 μM) for 8 hr, after which total RNA and whole cellular proteins were isolated. Cyclooxygenase-1, -2, and -3 RNA and protein levels were quantified using Northern and Western immunoassay. Results: IL-1β-, H 2O2-, TNF-α-, TNF-α + H2O 2-, or A2E-stressed ARPE-19 or HN cells displayed no significant up-regulation in COX-1 or COX-3 RNA message abundance; however, significant upregulation was observed in COX-2 RNA message and protein abundance. A2E treatment of HN cells resulted in modest increases in COX-3 protein, an effect that was not observed in ARPE-19 cells. Conclusions: COX-2 RNA levels were induced in cytokine-, peroxide-, and A2E-stressed ARPE-19 and HN cells. Lack of induction of COX-3 RNA message by A2E, coupled with increases in COX-3 protein under identical treatment conditions, suggest that significant post-transcriptional or post-translational controls may regulate COX-3 gene expression in HN cells. Stress-induced upregulation of COX-2 gene expression in ARPE-19 and HN cells may play a mechanistic role in promoting proinflammatory and/or pro-oxidative pathology in these tissues.",
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AU - Lukiw, Walter J.

AU - Mukherjee, Pranab K.

AU - Cui, Jian Guo

AU - Bazan, Nicolas G.

PY - 2006/3/1

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N2 - Purpose: To investigate the expression of cyclooxygenase (COX)-1, -2, and -3 RNA and protein in retinal pigment epithelial (ARPE-19) cells and in human neural (HN) cells exposed to the stress-inducing cytokines IL-1β and TNF-α, the oxidizing peroxide H2O2, the combination of TNF-α + H2O2, and the lipofuscin fluorophore A2E. Methods: Three-week-old ARPE-19 and HN cells were incubated with IL-1β (10 ng/ml), TNF-α (10 ng/ml), H2O2 (0.6 μM), TNF-α + H2O2 (10 ng/ml and 0.6 μM), or A2E (10 μM) for 8 hr, after which total RNA and whole cellular proteins were isolated. Cyclooxygenase-1, -2, and -3 RNA and protein levels were quantified using Northern and Western immunoassay. Results: IL-1β-, H 2O2-, TNF-α-, TNF-α + H2O 2-, or A2E-stressed ARPE-19 or HN cells displayed no significant up-regulation in COX-1 or COX-3 RNA message abundance; however, significant upregulation was observed in COX-2 RNA message and protein abundance. A2E treatment of HN cells resulted in modest increases in COX-3 protein, an effect that was not observed in ARPE-19 cells. Conclusions: COX-2 RNA levels were induced in cytokine-, peroxide-, and A2E-stressed ARPE-19 and HN cells. Lack of induction of COX-3 RNA message by A2E, coupled with increases in COX-3 protein under identical treatment conditions, suggest that significant post-transcriptional or post-translational controls may regulate COX-3 gene expression in HN cells. Stress-induced upregulation of COX-2 gene expression in ARPE-19 and HN cells may play a mechanistic role in promoting proinflammatory and/or pro-oxidative pathology in these tissues.

AB - Purpose: To investigate the expression of cyclooxygenase (COX)-1, -2, and -3 RNA and protein in retinal pigment epithelial (ARPE-19) cells and in human neural (HN) cells exposed to the stress-inducing cytokines IL-1β and TNF-α, the oxidizing peroxide H2O2, the combination of TNF-α + H2O2, and the lipofuscin fluorophore A2E. Methods: Three-week-old ARPE-19 and HN cells were incubated with IL-1β (10 ng/ml), TNF-α (10 ng/ml), H2O2 (0.6 μM), TNF-α + H2O2 (10 ng/ml and 0.6 μM), or A2E (10 μM) for 8 hr, after which total RNA and whole cellular proteins were isolated. Cyclooxygenase-1, -2, and -3 RNA and protein levels were quantified using Northern and Western immunoassay. Results: IL-1β-, H 2O2-, TNF-α-, TNF-α + H2O 2-, or A2E-stressed ARPE-19 or HN cells displayed no significant up-regulation in COX-1 or COX-3 RNA message abundance; however, significant upregulation was observed in COX-2 RNA message and protein abundance. A2E treatment of HN cells resulted in modest increases in COX-3 protein, an effect that was not observed in ARPE-19 cells. Conclusions: COX-2 RNA levels were induced in cytokine-, peroxide-, and A2E-stressed ARPE-19 and HN cells. Lack of induction of COX-3 RNA message by A2E, coupled with increases in COX-3 protein under identical treatment conditions, suggest that significant post-transcriptional or post-translational controls may regulate COX-3 gene expression in HN cells. Stress-induced upregulation of COX-2 gene expression in ARPE-19 and HN cells may play a mechanistic role in promoting proinflammatory and/or pro-oxidative pathology in these tissues.

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KW - COX-3

KW - Cyclooxygenase

KW - Human neural (HN) cells

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