Corbi, Samia C. T.
de Vasconcellos, Jaira F.
[3, 4, 5]
Bastos, Alliny S.
Bussaneli, Diego Girotto
da Silva, Barbara Roque
Santos, Raquel Alves
Takahashi, Catarina S.
Rocha, Cristiane de S.
Carvalho, Benilton de Sa
Maurer-Morelli, V, Claudia
Orrico, Silvana R. P.
[1, 6, 12]
Barros, Silvana P.
Scarel-Caminaga, Raquel M.
 Henry Jackson Fdn Adv Mil Med, Bethesda, MD - USA
 Orrico, Silvana R. P., Union Coll Great Lakes UNILAGO, Adv Res Ctr Med, BR-15030070 Sao Jose Do Rio Preto, SP, Brazil.Corbi, Samia C. T., UNESP Sao Paulo State Univ, Sch Dent Araraquara, Dept Diag & Surg, BR-14801385 Araraquara, SP - Brazil
 Univ Franca, Postgrad Program Sci, BR-14404600 Franca, SP - Brazil
 Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Genet, BR-14049900 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Fac Philosophy Sci & Letters Ribeirao Preto, Dept Biol, BR-14049900 Ribeirao Preto, SP - Brazil
 V, Univ Campinas UNICAMP, Dept Med Genet & Med Genom, BR-13083887 Campinas, SP - Brazil
 Univ Estadual Campinas, Dept Stat, Inst Math Stat & Sci Comp, BR-13083859 Campinas, SP - Brazil
 Union Coll Great Lakes UNILAGO, Adv Res Ctr Med, BR-15030070 Sao Jose Do Rio Preto, SP - Brazil
 Univ N Carolina, Dept Periodontol, Sch Dent, Chapel Hill, NC 27515 - USA
Total Affiliations: 13
MAY 18 2020.
Web of Science Citations:
Type 2 diabetes mellitus (T2DM), dyslipidemia and periodontitis are frequently associated pathologies; however, there are no studies showing the peripheral blood transcript profile of these combined diseases. Here we identified the differentially expressed genes (DEGs) of circulating lymphocytes and monocytes to reveal potential biomarkers that may be used as molecular targets for future diagnosis of each combination of these pathologies (compared to healthy patients) and give insights into the underlying molecular mechanisms of these diseases. Study participants (n=150) were divided into groups: (H) systemically and periodontal healthy (control group); (P) with periodontitis, but systemically healthy; (DL-P) with dyslipidemia and periodontitis; (T2DMwell-DL-P) well-controlled type 2 diabetes mellitus with dyslipidemia and periodontitis; and (T2DMpoorly-DL-P) poorly-controlled type 2 diabetes mellitus with dyslipidemia and periodontitis. We preprocessed the microarray data using the Robust Multichip Average (RMA) strategy, followed by the RankProd method to identify candidates for DEGs. Furthermore, we performed functional enrichment analysis using Ingenuity Pathway Analysis and Gene Set Enrichment Analysis. DEGs were submitted to pairwise comparisons, and selected DEGs were validated by quantitative polymerase chain reaction. Validated DEGs verified from T2DMpoorly-DL-P versus H were: TGFB1I1, VNN1, HLADRB4 and CXCL8; T2DMwell-DL-P versus H: FN1, BPTF and PDE3B; DL-P versus H: DAB2, CD47 and HLADRB4; P versus H: IGHDL-P, ITGB2 and HLADRB4. In conclusion, we identified that circulating lymphocytes and monocytes of individuals simultaneously affected by T2DM, dyslipidemia and periodontitis, showed an altered molecular profile mainly associated to inflammatory response, immune cell trafficking, and infectious disease pathways. Altogether, these results shed light on novel potential targets for future diagnosis, monitoring or development of targeted therapies for patients sharing these conditions. (AU)