Profiling of Differentially Expressed Genes in Human Polymorphonuclear Leukocyte on Human Amniotic Membrane.
- Author:
Hyoung Kyun KIM
1
;
Gyu Heon HAN
;
Tae Hoon CHOI
Author Information
1. Department of Ophthalmology, Kangdong Sacred Heart Hospital, Hallym University College of Medicine, Korea. thc@hallym.or.kr
- Publication Type:Original Article
- Keywords:
Amniotic membrane;
cDNA microarray;
Inflammation;
Polymorphonuclear cell
- MeSH:
Amnion*;
Antigens, Surface;
Apoptosis;
Chemokine CCL5;
Chemokines;
Cytokines;
DNA;
DNA Probes;
DNA, Complementary;
DNA-Binding Proteins;
Humans*;
Inflammation;
Membranes;
Neutrophils*;
Oligonucleotide Array Sequence Analysis;
Oncostatin M;
Plastics;
RNA;
Transcription Factors;
Transforming Growth Factor beta
- From:Journal of the Korean Ophthalmological Society
2003;44(11):2615-2626
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: To identify genes that showed altered expression between human polymorphonuclear (PMN) cell cultured on plastic and on amniotic membrane by the technique of differential hybridization of two Altas(TM) Human cDNA expression array. METHODS: 32P-labeled complimentary DNA probes derived from RNA of either human polymorphonuclear leukocyte cultured on plastic and cultured on amniotic membrane were hybridized to two identical human cDNA expression array membranes containing 588 known genes. RESULTS: Of the total 588 genes, 130 genes were up- or down-regulated. 50 up-regulated and 80 down-regulated genes were identified in polymorphonuclear leukocyte cultured on amniotic membrane compared with control. After different signal intensity was normalized more than 4000 by Atlas Image(TM) 1.0 Software, 19 genes were up-regulated and 36 genes down-regulated. CONCLUSIONS: Genes associated with the process of apoptosis, DNA synthesis and repair were down-regulated in PMN cultured on AM and genes associated with DNA binding protein, transcription factor were altered. Cell-cell communication factors including TGF-beta, PDGF-A, RANTES, MRP-14, oncostatin M, MIP-2 alpha were significantly down-regulated and cell surface antigen CD11a (LFA-1) was down-regulated, suggesting that AM can suppress the inflammatory reaction mediated by adhesion molecule, inflammatory, proinflammatory cytokines and chemokines.
