title: Transcriptome analysis reveals mucin 4 to be highly associated with periodontitis and identifies pleckstrin as a link to systemic diseases.
abstract: The multifactorial chronic inflammatory disease periodontitis, which is characterized by destruction of tooth-supporting tissues, has also been implicated as a risk factor for various systemic diseases. Although periodontitis has been studied extensively, neither disease-specific biomarkers nor therapeutic targets have been identified, nor its link with systemic diseases. Here, we analyzed the global transcriptome of periodontitis and compared its gene expression profile with those of other inflammatory conditions, including cardiovascular disease (CVD), rheumatoid arthritis (RA), and ulcerative colitis (UC). Gingival biopsies from 62 patients with periodontitis and 62 healthy subjects were subjected to RNA sequencing. The up-regulated genes in periodontitis were related to inflammation, wounding and defense response, and apoptosis, whereas down-regulated genes were related to extracellular matrix organization and structural support. The most highly up-regulated gene was mucin 4 (MUC4), and its protein product was confirmed to be over-expressed in periodontitis. When comparing the expression profile of periodontitis with other inflammatory diseases, several gene ontology categories, including inflammatory response, cell death, cell motion, and homeostatic processes, were identified as common to all diseases. Only one gene, pleckstrin (PLEK), was significantly overexpressed in periodontitis, CVD, RA, and UC, implicating this gene as an important networking link between these chronic inflammatory diseases.
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Anna
authors.initials: A
authors.lastname: Lundmark
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Haleh
authors.initials: H
authors.lastname: Davanian
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Tove
authors.initials: T
authors.lastname: Båge
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Gunnar
authors.initials: G
authors.lastname: Johannsen
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Catalin
authors.initials: C
authors.lastname: Koro
authors.affiliation: KTH Royal Institute of Technology, Science for Life Laboratory, School of Biotechnology, Division of Gene Technology, SE-171 65 Solna, Sweden.
authors.forename: Joakim
authors.initials: J
authors.lastname: Lundeberg
authors.affiliation: Department of Dental Medicine, Division of Periodontology, Karolinska Institutet, SE-141 04 Huddinge, Sweden.
authors.forename: Tülay
authors.initials: T
authors.lastname: Yucel-Lindberg
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000473:pathology; D001798:Blood Proteins / Q000096:biosynthesis* / Q000235:genetics; D002318:Cardiovascular Diseases / Q000235:genetics / Q000473:pathology; D003093:Colitis, Ulcerative / Q000235:genetics / Q000473:pathology; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D008875:Middle Aged; D055264:Mucin-4 / Q000096:biosynthesis* / Q000235:genetics; D010518:Periodontitis / Q000235:genetics* / Q000473:pathology; D010750:Phosphoproteins / Q000096:biosynthesis* / Q000235:genetics; D059467:Transcriptome / Q000235:genetics*
chemical_list: D001798:Blood Proteins; D055264:Mucin-4; D010750:Phosphoproteins; C039077:platelet protein P47