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Differential gene expression in neutrophils from patients with generalized aggressive periodontitis
Author(s) -
Kubota Takehiko,
Morozumi Toshiya,
Shimizu Kunihiko,
Sugita Noriko,
Kobayashi Tetsuo,
Yoshie Hiromasa
Publication year - 2001
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2001.360607.x
Subject(s) - gene , chronic periodontitis , gene expression , microbiology and biotechnology , immunology , biology , transcription factor , medicine , periodontitis , genetics
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‐1β and VEGF genes, were expressed at a significantly higher level in Aggressive‐P and Chronic‐P than H ( p <0.01, 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‐β) and muskelin (cellular adhesion).