The Expression of Inflammatory Genes Is Upregulated in Peripheral Blood of Patients With Type 1 Diabetes
Our previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression cha...
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| Published in | Diabetes care Vol. 36; no. 9; pp. 2794 - 2802 |
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| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.09.2013
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0149-5992 1935-5548 1935-5548 |
| DOI | 10.2337/dc12-1986 |
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| Abstract | Our previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression changes in diabetes complications. RESEARCH DESIGH AND METHODS: We performed high-throughput real-time RT-PCR to validate gene expression changes in peripheral blood mononuclear cells (PBMCs) from a large sample set of 928 T1D patients and 922 control subjects.
Of the 18 genes analyzed here, eight genes (S100A8, S100A9, MNDA, SELL, TGFB1, PSMB3, CD74, and IL12A) had higher expression and three genes (GNLY, PSMA4, and SMAD7) had lower expression in T1D patients compared with control subjects, indicating that genes involved in inflammation, immune regulation, and antigen processing and presentation are significantly altered in PBMCs from T1D patients. Furthermore, one adhesion molecule (SELL) and three inflammatory genes mainly expressed by myeloid cells (S100A8, S100A9, and MNDA) were significantly higher in T1D patients with complications (odds ratio [OR] 1.3-2.6, adjusted P value = 0.005-10(-8)), especially those patients with neuropathy (OR 4.8-7.9, adjusted P value <0.005).
These findings suggest that inflammatory mediators secreted mainly by myeloid cells are implicated in T1D and its complications. |
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| AbstractList | Our previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression changes in diabetes complications. RESEARCH DESIGH AND METHODS: We performed high-throughput real-time RT-PCR to validate gene expression changes in peripheral blood mononuclear cells (PBMCs) from a large sample set of 928 T1D patients and 922 control subjects.
Of the 18 genes analyzed here, eight genes (S100A8, S100A9, MNDA, SELL, TGFB1, PSMB3, CD74, and IL12A) had higher expression and three genes (GNLY, PSMA4, and SMAD7) had lower expression in T1D patients compared with control subjects, indicating that genes involved in inflammation, immune regulation, and antigen processing and presentation are significantly altered in PBMCs from T1D patients. Furthermore, one adhesion molecule (SELL) and three inflammatory genes mainly expressed by myeloid cells (S100A8, S100A9, and MNDA) were significantly higher in T1D patients with complications (odds ratio [OR] 1.3-2.6, adjusted P value = 0.005-10(-8)), especially those patients with neuropathy (OR 4.8-7.9, adjusted P value <0.005).
These findings suggest that inflammatory mediators secreted mainly by myeloid cells are implicated in T1D and its complications. Our previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression changes in diabetes complications. RESEARCH DESIGH AND METHODS: We performed high-throughput real-time RT-PCR to validate gene expression changes in peripheral blood mononuclear cells (PBMCs) from a large sample set of 928 T1D patients and 922 control subjects.OBJECTIVEOur previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression changes in diabetes complications. RESEARCH DESIGH AND METHODS: We performed high-throughput real-time RT-PCR to validate gene expression changes in peripheral blood mononuclear cells (PBMCs) from a large sample set of 928 T1D patients and 922 control subjects.Of the 18 genes analyzed here, eight genes (S100A8, S100A9, MNDA, SELL, TGFB1, PSMB3, CD74, and IL12A) had higher expression and three genes (GNLY, PSMA4, and SMAD7) had lower expression in T1D patients compared with control subjects, indicating that genes involved in inflammation, immune regulation, and antigen processing and presentation are significantly altered in PBMCs from T1D patients. Furthermore, one adhesion molecule (SELL) and three inflammatory genes mainly expressed by myeloid cells (S100A8, S100A9, and MNDA) were significantly higher in T1D patients with complications (odds ratio [OR] 1.3-2.6, adjusted P value = 0.005-10(-8)), especially those patients with neuropathy (OR 4.8-7.9, adjusted P value <0.005).RESULTSOf the 18 genes analyzed here, eight genes (S100A8, S100A9, MNDA, SELL, TGFB1, PSMB3, CD74, and IL12A) had higher expression and three genes (GNLY, PSMA4, and SMAD7) had lower expression in T1D patients compared with control subjects, indicating that genes involved in inflammation, immune regulation, and antigen processing and presentation are significantly altered in PBMCs from T1D patients. Furthermore, one adhesion molecule (SELL) and three inflammatory genes mainly expressed by myeloid cells (S100A8, S100A9, and MNDA) were significantly higher in T1D patients with complications (odds ratio [OR] 1.3-2.6, adjusted P value = 0.005-10(-8)), especially those patients with neuropathy (OR 4.8-7.9, adjusted P value <0.005).These findings suggest that inflammatory mediators secreted mainly by myeloid cells are implicated in T1D and its complications.CONCLUSIONSThese findings suggest that inflammatory mediators secreted mainly by myeloid cells are implicated in T1D and its complications. Our previous gene expression microarray studies identified a number of genes differentially expressed in patients with type 1 diabetes (T1D) and islet autoantibody-positive subjects. This study was designed to validate these gene expression changes in T1D patients and to identify gene expression changes in diabetes complications. We performed high-throughput real-time RT-PCR to validate gene expression changes in peripheral blood mononuclear cells (PBMCs) from a large sample set of 928 T1D patients and 922 control subjects. Of the 18 genes analyzed here, eight genes (S100A8, S100A9, MNDA, SELL, TGFB1, PSMB3, CD74, and IL12A) had higher expression and three genes (GNLY, PSMA4, and SMAD7) had lower expression in T1D patients compared with control subjects, indicating that genes involved in inflammation, immune regulation, and antigen processing and presentation are significantly altered in PBMCs from T1D patients. Furthermore, one adhesion molecule (SELL) and three inflammatory genes mainly expressed by myeloid cells (S100A8, S100A9, and MNDA) were significantly higher in T1D patients with complications (odds ratio [OR] 1.3-2.6, adjusted P value = 0.005-10...), especially those patients with neuropathy (OR 4.8-7.9, adjusted P value <0.005). These findings suggest that inflammatory mediators secreted mainly by myeloid cells are implicated in T1D and its complications. (ProQuest: ... denotes formulae/symbols omitted.) |
| Audience | Professional |
| Author | Carey, Colleen Bode, Bruce Anderson, Stephen W. Robertson, David G. Steed, R. Dennis Hopkins, Diane Sharma, Ashok Jin, Yulan Reed, John Chip Wang, Xiaoxiao Steed, Leigh She, Jin-Xiong |
| Author_xml | – sequence: 1 givenname: Yulan surname: Jin fullname: Jin, Yulan organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, Department of Pathology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 2 givenname: Ashok surname: Sharma fullname: Sharma, Ashok organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, Department of Pathology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 3 givenname: Colleen surname: Carey fullname: Carey, Colleen organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 4 givenname: Diane surname: Hopkins fullname: Hopkins, Diane organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 5 givenname: Xiaoxiao surname: Wang fullname: Wang, Xiaoxiao organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 6 givenname: David G. surname: Robertson fullname: Robertson, David G. organization: Atlanta Diabetes Associates, Atlanta, Georgia – sequence: 7 givenname: Bruce surname: Bode fullname: Bode, Bruce organization: Atlanta Diabetes Associates, Atlanta, Georgia – sequence: 8 givenname: Stephen W. surname: Anderson fullname: Anderson, Stephen W. organization: Pediatric Endocrine Associates, Atlanta, Georgia – sequence: 9 givenname: John Chip surname: Reed fullname: Reed, John Chip organization: Southeastern Endocrine and Diabetes, Atlanta, Georgia – sequence: 10 givenname: R. Dennis surname: Steed fullname: Steed, R. Dennis organization: Southeastern Endocrine and Diabetes, Atlanta, Georgia – sequence: 11 givenname: Leigh surname: Steed fullname: Steed, Leigh organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia – sequence: 12 givenname: Jin-Xiong surname: She fullname: She, Jin-Xiong organization: Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Georgia Regents University, Augusta, Georgia, Department of Pathology, Medical College of Georgia, Georgia Regents University, Augusta, Georgia |
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| Keywords | Endocrinopathy Human Immunopathology Nutrition Patient Autoimmune disease Metabolic diseases Inflammation Gene expression Blood Gene Type 1 diabetes Genetics Endocrinology |
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| SubjectTerms | Adolescent Adult Aged Aged, 80 and over Antigens, Differentiation, B-Lymphocyte - genetics Antigens, Differentiation, Myelomonocytic - genetics Autoantibodies Autoimmunity Biological and medical sciences Calgranulin A - genetics Calgranulin B - genetics Cells Child Child, Preschool Cholesterol Diabetes Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diabetes. Impaired glucose tolerance Diabetics Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gene expression Genes Genetic aspects Histocompatibility Antigens Class II - genetics Humans Interleukin-12 Subunit p35 - genetics L-Selectin - genetics Leukocytes, Mononuclear - metabolism Male Medical sciences Metabolic diseases Middle Aged Miscellaneous Oligonucleotide Array Sequence Analysis Original Research Polymerase chain reaction Public health. Hygiene Public health. Hygiene-occupational medicine Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Transcription Factors - genetics Transforming Growth Factor beta1 - genetics Type 1 diabetes Up-Regulation - genetics Up-Regulation - physiology Young Adult |
| Title | The Expression of Inflammatory Genes Is Upregulated in Peripheral Blood of Patients With Type 1 Diabetes |
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