Differential gene expression in neutrophils from patients with generalized aggressive periodontitis.
Differential gene expression was investigated in neutrophils stimulated with N-formyl-methionyl-leucyl-phenylalanine using RNA fingerprinting by arbitrarily primed polymerase chain reaction (RAP-PCR). The cells were isolated from 3 groups of subjects: patients with generalized aggressive periodontitis (Aggressive-P. n = 6), generalized chronic periodontitis (Chronic-P, n = 6) and healthy controls (H, n = 8). Our results show that 37 genes were upregulated. while 27 genes were down-regulated in all Aggressive-P neutrophils by using RAP-PCR with 45 primer pairs. Reverse transcription-PCR analyses revealed that mRNA levels were significantly different (p<0.05) for heat shock transcription factor 4b (HSF4b) gene. Kruppel-like zinc finger transcription factor 9 (Zf9) and muskelin genes. HSF4b was greater in neutrophils from Aggressive-P compared to groups H and Chronic-P. Zf9 and muskelin genes were lower in Aggressive-P compared to the H groups, but no significant difference was noted compared to the Chronic-P group. The control genes, IL-1beta and VEGF genes, were expressed at a significantly higher level in Aggressive-P and Chronic-P than H (p<.01, p<0.05). In conclusion, the RAP-PCR technique used in this study enabled us to identify 3 Aggressive-P related genes, which had not been reported previously. Neutrophil functions in Aggressive-P patients are suggested to be altered by regulatory factors of the immune system including HSF4b (transcription factor), Zf9 (activator of TGF-beta) and muskelin (cellular adhesion).
Kubota
T
T
Department of Periodontology, Faculty of Dentistry, Niigata University, Niigata, Japan.
Morozumi
T
T
Shimizu
K
K
Sugita
N
N
Kobayashi
T
T
Yoshie
H
H
D000328:Adult; D010520:Aggressive Periodontitis / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D054637:Dual-Specificity Phosphatases; D005260:Female; D015870:Gene Expression; D000076249:Heat Shock Transcription Factors; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D047908:Intracellular Signaling Peptides and Proteins; D000075723:Kruppel-Like Factor 6; D051741:Kruppel-Like Transcription Factors; D008297:Male; D054639:Mitogen-Activated Protein Kinase Phosphatases; D009504:Neutrophils / Q000378:metabolism; D010518:Periodontitis / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D025221:Phosphofructokinases / Q000096:biosynthesis / Q000235:genetics; D014176:Protein Biosynthesis; D017027:Protein Tyrosine Phosphatases / Q000096:biosynthesis / Q000235:genetics; D011506:Proteins / Q000235:genetics; D011518:Proto-Oncogene Proteins; D012313:RNA / Q000032:analysis; D019105:Random Amplified Polymorphic DNA Technique; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D015534:Trans-Activators / Q000096:biosynthesis / Q000235:genetics; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics
D015815:Cell Adhesion Molecules; D004268:DNA-Binding Proteins; C486399:GREM1 protein, human; C102948:HSF4 protein, human; D000076249:Heat Shock Transcription Factors; C484462:Hsf4 protein, mouse; D036341:Intercellular Signaling Peptides and Proteins; D047908:Intracellular Signaling Peptides and Proteins; C105465:KLF6 protein, human; C491358:Klf6 protein, mouse; D000075723:Kruppel-Like Factor 6; D051741:Kruppel-Like Transcription Factors; C503019:MKLN1 protein, human; C503020:Mkln1 protein, mouse; D011506:Proteins; D011518:Proto-Oncogene Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D012313:RNA; D025221:Phosphofructokinases; C120407:DUSP10 protein, human; D054639:Mitogen-Activated Protein Kinase Phosphatases; D054637:Dual-Specificity Phosphatases; D017027:Protein Tyrosine Phosphatases