ABSTRACT
<p><b>OBJECTIVE</b>To investigate promoter methylation status of LITAF gene in B-cell lymphoma and to explore transcription regulation of 5-Aza-2'-deoxycytidine (5-Aza-CdR) on LITAF gene.</p><p><b>METHODS</b>One hundred and five paraffin specimens including 54 cases of diffuse large B cell lymphoma (DLBCL), 15 small lymphocytic lymphoma (SLL), 8 mucosa-associated lymphoid tissue lymphoma (MALT) and 6 follicular lymphoma (FL) were included. Five reactive lymphoid hyperplasia samples were collected as control. Methylation status of CpG island in LITAF gene in the specimens and in Raji, Pfeiffer and Daudi cell lines were detected by methylation-specific PCR (MSP). LITAF expression in Raji, Pfeiffer and Daudi cell lines with or without 5-Aza-CdR treatment was detected by Western blot and immunohistochemistry. The inhibitory ratio in the three cell lines was measured by MTT assay.</p><p><b>RESULTS</b>The frequency of LITAF gene methylation in B-cell lymphoma was 89.5% (94/105) . Among them, 3.8% (4/105) showed complete hypermethylation. In control group, however, there was no methylation in CpG island of LITAF gene promoter. The expression of LITAF was recovered or increased along with the cell growth inhibition when the cells exposed to demethylating reagent.</p><p><b>CONCLUSIONS</b>LITAF gene silencing with aberrant CpG methylation is probably one of the critical events to the oncogenesis of B-cell lymphoma, which may have important implications as a candidate marker for diagnosis and target gene therapy.</p>
Subject(s)
Adult , Humans , Azacitidine , Metabolism , Cell Line, Tumor , CpG Islands , DNA Methylation , Gene Silencing , Lymphoma, B-Cell , Genetics , Metabolism , Lymphoma, B-Cell, Marginal Zone , Genetics , Lymphoma, Large B-Cell, Diffuse , Genetics , Nuclear Proteins , Genetics , Metabolism , Polymerase Chain Reaction , Promoter Regions, Genetic , Transcription Factors , Genetics , MetabolismABSTRACT
Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination compound on sodium current in single rat ventricular myocytes of arrhythmia induced by aconitine.Methods Whole-cell patch clamp was used to record INa in normal cardiomyocytes and single rat ventricular cardiomyocytes of arrhythmia induced by aconitine.Results In ventricular cardiomyocytes of rat,INa was blocked by 100~400 ?mol?L-1 TMCC in a concentration-dependent manner.INa was increasd from(45.56?1.96)pA/pF to(59.19?11.49)pA/pF by 1 ?mol?L-1 aconitine,while decreased to(34.23?1.33)pA/pF by 24.24 ?mol?L-1 amiodarone.TMCC(100,200,400 ?mol?L-1)could restore INa to(51.61?5.96)pA/pF,(40.91?6.73)pA/pF,(41.50?5.50)pA/pF respectively.Amiodarone could restore INa to(40.22?1.47)pA/pF.Conclusions TMCC can restore INa,which is increased by aconitine,and the effect is equal to that of amiodarone.TMCC blocks INa of ventricular cardiomyocytes,which may be one of its antiarrhythmic mechanisms.