ABSTRACT
Chronic caffeine exposure during pregnancy has an effect on fetal growth; however, the adverse effects of caffeine on embryogenesis are not well understood and controversial. We used cDNA microarray technology to determine whether caffeine alters gene expressions in a human cytotrophoblast-like cell line, BeWo. We found that the expression of the B-cell CLL/lymphoma 2 (Bcl-2) gene in BeWo cells was down-regulated by caffeine, suggesting that chronic exposure during the gestational period could exert an influence on embryogenesis. We then focused on the Bcl-2- and Bcl-2-associated X protein gene, Bax, to study the responsive gene expression in BeWo cells as well as placentas of pregnant rats fed a diet supplemented with caffeine (2 mg/100 g body weight) during gestation, and analyzed the gene expressions using LightCycler-based quantitative real-time polymerase chain reaction assays. We found a significantly decreased level of Bcl-2 mRNA expression, which demonstrated the influence of caffeine on placental function.
Subject(s)
Caffeine/pharmacology , Gene Expression Regulation/drug effects , Placenta/drug effects , Proto-Oncogene Proteins c-bcl-2/genetics , RNA, Messenger/metabolism , Animals , Base Sequence , Cell Line , DNA Primers , Female , Placenta/metabolism , Pregnancy , RNA, Messenger/genetics , RatsABSTRACT
It is well known that Down syndrome (DS) is a premature ageing syndrome. Periodontal disease in individuals with DS develops rapidly and extensively in a relatively younger age bracket compared with that in healthy controls. The mechanisms involved in the periodontal inflammatory processes in DS patients are not fully understood. In the present study, the non-inflamed gingival fibroblasts isolated from seven patients with DS (DGF) and seven healthy controls (NDGF) were stimulated with lipopolysaccharide (LPS) derived from Actinobacillus actinomycetemcomitans (A. a.). We measured the level of prostaglandin E2 (PGE2) production by DGF and NDGF by radioimmunoassay, and also measured the mRNA expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) by using the real-time PCR method. We found the higher levels of LPS-stimulated COX-2 mRNA expression and PGE2 production in DGF when compared with those in NDGF. This study may indicate that overexpression of LPS-stimulated COX-2 induced a greater ability of DGF to produce PGE2, and that these phenomena may be responsible for the severer periodontal disease in DS patients.
