期刊
JAPANESE JOURNAL OF OPHTHALMOLOGY
卷 55, 期 4, 页码 405-410出版社
SPRINGER TOKYO
DOI: 10.1007/s10384-011-0030-6
关键词
Interleukin-4 receptor alpha (IL-4R alpha); Human corneal epithelial cells; Interleukin-4 (IL-4); Interleukin-13 (IL-13)
资金
- Japanese Ministry of Health, Labour and Welfare
- Japanese Ministry of Education, Culture, Sports, Science and Technology
- CREST from JST
- Kyoto Foundation for the Promotion of Medical Science
- Kyoto Prefectural University of Medicine
- Shiseido Female Researcher Science Grant
- Japan Allergy Foundation
- Grants-in-Aid for Scientific Research [22390325] Funding Source: KAKEN
We previously reported that human conjunctival epithelial cells expressed functioning interleukin-4 receptor alpha (IL-4R alpha). In this study, we investigated whether human corneal epithelial cells also express functioning IL-4R alpha. The presence of IL-4R alpha mRNA and protein in human corneal epithelium was examined by reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistology, respectively. The cell surface expression of IL-4R alpha and the transcripts upregulated upon IL-4R alpha ligand (IL-4 or IL-13) stimulation were examined by flow cytometry and quantitative RT-PCR, respectively, using immortalized human corneal-limbal epithelial (HCLE) cells. The mRNA and protein of IL-4R alpha were detected in human corneal epithelium. Flow cytometry analysis showed the cell surface expression of IL-4R alpha protein. Quantitative RT-PCR assay of HCLE cells showed the upregulation of the transcripts tumor necrosis factor alpha-induced protein 6 (TNFAIP6), RAS guanyl-releasing protein 1 (RASGRP1), carbonic anhydrase II (CA2), cytokine-inducible SH2-containing protein (CISH), hyaluronan synthase 3 (HAS3), calpain 14 (CAPN14), endothelin receptor type A (EDNRA), cathepsin C (CTSC), and lecithin retinol acyltransferase (LRAT) as well as human conjunctival epithelial cells. Human corneal epithelial cells expressed functioning IL-4R alpha, and stimulation of its ligands, IL-4 and IL-13, could induce the expression of various genes, e.g., antiinflammatory molecule genes such as TNFAIP6 and CISH and cellular differentiation and proliferation-related molecule genes such as RASGRP1, HAS3, EDNRA, and LRAT.
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