PMID- 14655518 OWN - NLM STAT- MEDLINE DCOM- 20040116 LR - 20071114 IS - 1399-543X (Print) IS - 1399-543X (Linking) VI - 4 IP - 1 DP - 2003 Mar TI - Aberrant monocyte prostaglandin synthase 2 (PGS2) expression in type 1 diabetes before and after disease onset. PG - 10-8 AB - METHODS: We examined monocyte prostaglandin synthase 2 (PGS2/COX2) expression in individuals at risk for or with type 1 diabetes including: (i) 58 established type 1 and 2 diabetic patients; (ii) 34 autoantibody positive (AA+) children and adults; (iii) 164 infants and young children with insulin-dependent diabetes mellitus (IDDM) susceptibility human leukocyte antigen (HLA) alleles; and (iv) 37 healthy control individuals, over a 5-yr period. RESULTS: Established type 1 diabetic patients (1 month to 30+ yr post-disease onset) had significantly higher PGS2 expression than healthy controls; by contrast, insulin-treated type 2 diabetic patients had significantly lower PGS2 expression than healthy controls. Longitudinal studies of AA+ subjects at risk for type 1 diabetes indicated that 73% (11/15) of individuals who developed this disease during the study period expressed high levels of PGS2 prior to or after onset. We also found high level PGS2 expression in genetically at-risk infants and young children that correlated with having a first-degree relative with type 1 diabetes, but not with age, gender, or HLA genotype. In this population, high level PGS2 expression coincided with or preceded autoantibody detection in 30% (3/10) of subjects. CONCLUSIONS: These findings suggest that high level monocyte PGS2 expression, although subject to fluctuation, is present in at-risk subjects at an early age and is maintained during progression to and after type 1 diabetes onset. FAU - Litherland, S A AU - Litherland SA AD - Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Box 100275, JHMHC, Gainesville, Florida 32610, USA. FAU - She, J X AU - She JX FAU - Schatz, D AU - Schatz D FAU - Fuller, K AU - Fuller K FAU - Hutson, A D AU - Hutson AD FAU - Peng, R H AU - Peng RH FAU - Li, Y AU - Li Y FAU - Grebe, K M AU - Grebe KM FAU - Whittaker, D S AU - Whittaker DS FAU - Bahjat, K AU - Bahjat K FAU - Hopkins, D AU - Hopkins D FAU - Fang, Q AU - Fang Q FAU - Spies, P D AU - Spies PD FAU - North, K AU - North K FAU - Wasserfall, C AU - Wasserfall C FAU - Cook, R AU - Cook R FAU - Dennis, M A AU - Dennis MA FAU - Crockett, S AU - Crockett S FAU - Sleasman, J AU - Sleasman J FAU - Kocher, J AU - Kocher J FAU - Muir, A AU - Muir A FAU - Silverstein, J AU - Silverstein J FAU - Atkinson, M AU - Atkinson M FAU - Clare-Salzler, M J AU - Clare-Salzler MJ LA - eng GR - 1RO1HD 37800/HD/NICHD NIH HHS/United States GR - P01-AI42288-03/AI/NIAID NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - Denmark TA - Pediatr Diabetes JT - Pediatric diabetes JID - 100939345 RN - 0 (Autoantibodies) RN - 0 (HLA Antigens) RN - 0 (Isoenzymes) RN - 0 (Membrane Proteins) RN - EC 1.14.99.1 (Cyclooxygenase 2) RN - EC 1.14.99.1 (PTGS2 protein, human) RN - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases) SB - IM MH - Adult MH - Autoantibodies/blood MH - Child, Preschool MH - Cyclooxygenase 2 MH - Diabetes Mellitus, Type 1/*enzymology/genetics/immunology MH - Diabetes Mellitus, Type 2/enzymology MH - Female MH - Genetic Predisposition to Disease MH - Genotype MH - HLA Antigens/genetics MH - Humans MH - Infant MH - Isoenzymes/*blood MH - Male MH - Membrane Proteins MH - Monocytes/*enzymology MH - Prostaglandin-Endoperoxide Synthases/*blood EDAT- 2003/12/06 05:00 MHDA- 2004/01/17 05:00 CRDT- 2003/12/06 05:00 PHST- 2003/12/06 05:00 [pubmed] PHST- 2004/01/17 05:00 [medline] PHST- 2003/12/06 05:00 [entrez] AID - PDI042 [pii] AID - 10.1034/j.1399-5448.2003.00042.x [doi] PST - ppublish SO - Pediatr Diabetes. 2003 Mar;4(1):10-8. doi: 10.1034/j.1399-5448.2003.00042.x.