Anti-SVIL (aa 1679-1786) polyclonal antibody

In this issue of Molecular Cell, Laurent et al. (2015) demonstrated that a neuron-enriched isoform of LSD1 (LSD1+ 8a) within a SVIL-containing complex exhibits H3K9me1/2-specific demethylation activity. Such activity was crucial for gene activation during mammalian neurogenesis.

Differential gene expression was examined in human neutrophils stimulated with lipopolysaccharide front Porphyromonas gingivalis (P. gingivalis-LPS) using RNA fingerprinting by arbitrarily primed polymerase chain reaction (RAP-PCR). LPS from Escherichia coli (E. coli-LPS) was used as control. More than 200 differently expressed transcripts were found in X subjects showing differential regulation at the transcriptional level. Densitometric analyses revealed that 42-100 genes were upregulated. while 53 116 genes were downregulated by P. gingivalis-LPS compared with E, coli-LPS. The results of sequencing identification showed the presence of supervillin (SVIL) and vascular endothelial growth factor (VEGF) genes in the clones which were upregulated by P. gingivalis-LPS. Consequently. semiquantitative analyses proved that the level of mRNA for SVIL and VEGF were significantly higher in P. gingivalis-LPS-stimulated neutrophils than in other bacterial(E. coli. Actinobacillus actinomycetemcomitans. Prevotella intermedia) LPS- or synthetic lipid A-stimulated neutrophils. Our findings suggest that an elevated mRNA expression for SVIL could be associated with impaired function of neutrophils when stimulated by P. gingivalis-LPS. Further. the VEGF mRNA over-expression might be related to the pathogenesis of P. gingivalis-associated periodontitis. The RAP-PCR technique used in this study enabled us to identify a number of P. gingivalis-LPS regulated genes which hitherto have not been reported.