Esra Guzeldemir-Akcakanat1, Begum Alkan2, Deniz Sunnetci-Akkoyunlu3, Busra Gurel4, V Merve Balta1, Bahadir Kan5, Emel Akgun4, Elif Busra Yilmaz3, Ahmet Tarik Baykal4, Naci Cine3, Vakur Olgac6, Esen Gumuslu3, Hakan Savli3. 1. Department of Periodontology, Faculty of Dentistry, Kocaeli University, Kocaeli, Turkey. 2. Department of Periodontology, Faculty of Dentistry, Istanbul Medipol University, Istanbul, Turkey. 3. Department of Medical Genetics, Faculty of Medicine, Kocaeli University, Kocaeli, Turkey. 4. Department of Medical Biochemistry, School of Medicine, Acibadem Mehmet Ali Aydınlar University, Istanbul, Turkey. 5. Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Kocaeli University, Kocaeli, Turkey. 6. Department of Tumor Pathology, Institute of Oncology, Istanbul University, Istanbul, Turkey.
Abstract
BACKGROUND: To elucidate molecular signatures of chronic periodontitis (CP) using gingival tissue samples through omics-based whole-genome transcriptomic and whole protein profiling. METHODS: Gingival tissues from 18 CP and 25 controls were analyzed using gene expression microarrays to identify gene expression patterns and the proteins isolated from these samples were subjected to comparative proteomic analysis by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The data from transcriptomics and proteomics were integrated to reveal common shared genes and proteins. RESULTS: The most upregulated genes in CP compared with controls were found as MZB1, BMS1P20, IGLL1/IGLL5, TNFRSF17, ALDH1A1, KIAA0125, MMP7, PRL, MGC16025, ADAM11, and the most upregulated proteins in CP compared with controls were BPI, ITGAM, CAP37, PCM1, MMP-9, MZB1, UGTT1, PLG, RAB1B, HSP90B1. Functions of the identified genes were involved cell death/survival, DNA replication, recombination/repair, gene expression, organismal development, cell-to-cell signaling/interaction, cellular development, cellular growth/proliferation, cellular assembly/organization, cellular function/maintenance, cellular movement, B-cell development, and identified proteins were involved in protein folding, response to stress, single-organism catabolic process, regulation of peptidase activity, and negative regulation of cell death. The integration and validation analysis of the transcriptomics and proteomics data revealed two common shared genes and proteins, MZB1 and ECH1. CONCLUSION: Integrative data from transcriptomics and proteomics revealed MZB1 as a potent candidate for chronic periodontitis.
BACKGROUND: To elucidate molecular signatures of chronic periodontitis (CP) using gingival tissue samples through omics-based whole-genome transcriptomic and whole protein profiling. METHODS: Gingival tissues from 18 CP and 25 controls were analyzed using gene expression microarrays to identify gene expression patterns and the proteins isolated from these samples were subjected to comparative proteomic analysis by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The data from transcriptomics and proteomics were integrated to reveal common shared genes and proteins. RESULTS: The most upregulated genes in CP compared with controls were found as MZB1, BMS1P20, IGLL1/IGLL5, TNFRSF17, ALDH1A1, KIAA0125, MMP7, PRL, MGC16025, ADAM11, and the most upregulated proteins in CP compared with controls were BPI, ITGAM, CAP37, PCM1, MMP-9, MZB1, UGTT1, PLG, RAB1B, HSP90B1. Functions of the identified genes were involved cell death/survival, DNA replication, recombination/repair, gene expression, organismal development, cell-to-cell signaling/interaction, cellular development, cellular growth/proliferation, cellular assembly/organization, cellular function/maintenance, cellular movement, B-cell development, and identified proteins were involved in protein folding, response to stress, single-organism catabolic process, regulation of peptidase activity, and negative regulation of cell death. The integration and validation analysis of the transcriptomics and proteomics data revealed two common shared genes and proteins, MZB1 and ECH1. CONCLUSION: Integrative data from transcriptomics and proteomics revealed MZB1 as a potent candidate for chronic periodontitis.