Interleukin-1 receptor antagonist production in human and murine lens

M. C. Kennedy, S. R. Planck, J. C. Ansel, J. T. Rosenbaum

Research output: Contribution to journalArticlepeer-review

Abstract

Purpose: Interleukin-1 receptor antagonist (IL-1ra) can effectively reduce target cell response to interleukin-1 (IL-1) by competition for binding to the IL-1 type 1 receptor. We examined normal human and murine lenses as well as cultured lens epithelial cells for the expression of IL-1ra mRNA and the production of IL-1ra protein. Methods: Expression of IL-1ra mRNA was studied by reverse transcriptase polymerase chain reaction (RT-PCR) analysis of total RNA isolated from fresh human lens and cultured human lens epithelial cells. In situ RT-PCR technique was used to study the expression of IL-1ra mRNA by normal lenses. Quantitation of the IL-1ra protein produced by cultured lens epithelial cells was done by ELISA. Normal human lenses, obtained from eye bank donors, were examined by immunohistochemical staining of frozen sections. Results: Human lens epithelial cells showed constitutive IL-1ra protein and mRNA production. Stimulation by IL-1α of cultured cells upregulated IL-1ra mRNA levels and increased protein levels by 5-fold. IL-1ra specific in situ RT-PCR labeled all epithelial cells of normal murine lens. Immunohistochemical staining of the normal human lens showed positive staining thoughout the epithelium and in the lens fiber layer. Conclusion: IL-1ra is produced by the cells of human and murine lens epithelium. IL-1ra production by these cells is constitutive and can be upregulated by cytokines.

Original languageEnglish (US)
Pages (from-to)S989
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Fingerprint

Dive into the research topics of 'Interleukin-1 receptor antagonist production in human and murine lens'. Together they form a unique fingerprint.

Cite this