Journal of periodontology · 2008
Blood cell gene expression profiling in subjects with aggressive periodontitis and chronic arthritis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sørensen Lars K, Havemose-Poulsen Anne, Sønder Søren U, Bendtzen Klaus, Holmstrup Palle
Аннотация
BACKGROUND: Microarray analysis of local and peripheral cells in subjects with immune-inflammatory diseases may identify candidate genes associated with these diseases. The present study identified differentially expressed genes in peripheral blood mononuclear cells (PBMCs) from subjects with untreated localized aggressive periodontitis (LAgP) or generalized aggressive periodontitis (GAgP). Differentially expressed genes were validated in groups of subjects with LAgP, GAgP, juvenile idiopathic arthritis (JIA), or rheumatoid arthritis (RA) and controls.
METHODS: Candidate genes were identified by gene expression profiling of PBMCs using a microarray system in untreated gender-matched subjects with LAgP (N = 2) or GAgP (N = 3) and controls (N = 2) younger than 35 years of age. The microarray results were validated by real-time reverse transcription-polymerase chain reaction (RT-PCR) using PBMCs from 103 individuals, including groups of subjects with LAgP (N = 18), GAgP (N = 27), JIA (N = 10), or RA (N = 23) and controls (N = 25).
RESULTS: Of 53 differentially expressed candidate genes identified in subjects with LAgP, 14 were involved in immune responses and inflammatory processes. Of these, the RT-PCR validation confirmed that Toll-like receptor 2 gene (TLR2) and myomesin 2 gene had a significantly higher expression in subjects with LAgP than in controls. RT-PCR also showed increased expression of TLR2 in subjects with RA. Comparison of subjects with GAgP to controls using microarray analysis identified only three upregulated genes.
CONCLUSION: Several genes upregulated in subjects with LAgP were related to immune responses including TLR2 and myomesin 2.
METHODS: Candidate genes were identified by gene expression profiling of PBMCs using a microarray system in untreated gender-matched subjects with LAgP (N = 2) or GAgP (N = 3) and controls (N = 2) younger than 35 years of age. The microarray results were validated by real-time reverse transcription-polymerase chain reaction (RT-PCR) using PBMCs from 103 individuals, including groups of subjects with LAgP (N = 18), GAgP (N = 27), JIA (N = 10), or RA (N = 23) and controls (N = 25).
RESULTS: Of 53 differentially expressed candidate genes identified in subjects with LAgP, 14 were involved in immune responses and inflammatory processes. Of these, the RT-PCR validation confirmed that Toll-like receptor 2 gene (TLR2) and myomesin 2 gene had a significantly higher expression in subjects with LAgP than in controls. RT-PCR also showed increased expression of TLR2 in subjects with RA. Comparison of subjects with GAgP to controls using microarray analysis identified only three upregulated genes.
CONCLUSION: Several genes upregulated in subjects with LAgP were related to immune responses including TLR2 and myomesin 2.