title: Transcriptional profiling of human smooth muscle cells infected with gingipain and fimbriae mutants of Porphyromonas gingivalis.
abstract: Porphyromonas gingivalis (P. gingivalis) is considered to be involved in the development of atherosclerosis. However, the role of different virulence factors produced by P. gingivalis in this process is still uncertain. The aim of this study was to investigate the transcriptional profiling of human aortic smooth muscle cells (AoSMCs) infected with wild type, gingipain mutants or fimbriae mutants of P. gingivalis. AoSMCs were exposed to wild type (W50 and 381), gingipain mutants (E8 and K1A), or fimbriae mutants (DPG-3 and KRX-178) of P. gingivalis. We observed that wild type P. gingivalis changes the expression of a considerable larger number of genes in AoSMCs compare to gingipain and fimbriae mutants, respectively. The results from pathway analysis revealed that the common differentially expressed genes for AoSMCs infected by 3 different wild type P. gingivalis strains were enriched in pathways of cancer, cytokine-cytokine receptor interaction, regulation of the actin cytoskeleton, focal adhesion, and MAPK signaling pathway. Disease ontology analysis showed that various strains of P. gingivalis were associated with different disease profilings. Our results suggest that gingipains and fimbriae, especially arginine-specific gingipain, produced by P. gingivalis play important roles in the association between periodontitis and other inflammatory diseases, including atherosclerosis.
authors.affiliation: Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden.
authors.forename: Boxi
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden.
authors.forename: Allan
authors.initials: A
authors.lastname: Sirsjö
authors.affiliation: Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden.
authors.forename: Hazem
authors.initials: H
authors.lastname: Khalaf
authors.affiliation: Department of Clinical Medicine, School of Health Sciences, Örebro University, Örebro, Sweden.
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Bengtsson
mesh_terms: D008841:Actin Cytoskeleton / Q000235:genetics / Q000378:metabolism; D018829:Adhesins, Bacterial / Q000235:genetics*; D001011:Aorta / Q000166:cytology; D050197:Atherosclerosis / Q000235:genetics / Q000473:pathology; D002460:Cell Line; D003546:Cysteine Endopeptidases / Q000235:genetics*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D010861:Fimbriae, Bacterial / Q000235:genetics*; D022001:Focal Adhesions / Q000235:genetics / Q000378:metabolism; D020869:Gene Expression Profiling; D000080867:Gingipain Cysteine Endopeptidases; D006801:Humans; D020935:MAP Kinase Signaling System / Q000235:genetics; D009154:Mutation; D032389:Myocytes, Smooth Muscle / Q000166:cytology / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000472:pathogenicity*; D060888:Real-Time Polymerase Chain Reaction; D018121:Receptors, Cytokine / Q000235:genetics / Q000378:metabolism; D059467:Transcriptome
chemical_list: D018829:Adhesins, Bacterial; D016207:Cytokines; D000080867:Gingipain Cysteine Endopeptidases; D018121:Receptors, Cytokine; D003546:Cysteine Endopeptidases