This article is part of the supplement: The 2010 International Conference on Bioinformatics and Computational Biology (BIOCOMP 2010): Genomics
Transcriptomic profiles of peripheral white blood cells in type II diabetes and racial differences in expression profiles
1 Department of Biology, Tougaloo College, Tougaloo, MS 39174, USA
2 School of Computing, University of Southern Mississippi, Hattiesburg, MS 39406, USA
3 Department of Pathology, University of Mississippi Medical Center, Jackson, MS 39216, USA
4 Madden Medical Clinic,1071 East Franklin St, Carthage, MS 39051, USA
5 School of Medicine, University of Mississippi Medical Center, Jackson, MS 39216, USA
6 Wuhan University of Science and Technology, Wuhan, Hubei 430081, P.R. China
7 Department of Internal Medicine, Rush University Medical Center, Chicago, IL 60612, USA
BMC Genomics 2011, 12(Suppl 5):S12 doi:10.1186/1471-2164-12-S5-S12Published: 23 December 2011
Along with obesity, physical inactivity, and family history of metabolic disorders, African American ethnicity is a risk factor for type 2 diabetes (T2D) in the United States. However, little is known about the differences in gene expression and transcriptomic profiles of blood in T2D between African Americans (AA) and Caucasians (CAU), and microarray analysis of peripheral white blood cells (WBCs) from these two ethnic groups will facilitate our understanding of the underlying molecular mechanism in T2D and identify genetic biomarkers responsible for the disparities.
A whole human genome oligomicroarray of peripheral WBCs was performed on 144 samples obtained from 84 patients with T2D (44 AA and 40 CAU) and 60 healthy controls (28 AA and 32 CAU). The results showed that 30 genes had significant difference in expression between patients and controls (a fold change of <-1.4 or >1.4 with a P value <0.05). These known genes were mainly clustered in three functional categories: immune responses, lipid metabolism, and organismal injury/abnormaly. Transcriptomic analysis also showed that 574 genes were differentially expressed in AA diseased versus AA control, compared to 200 genes in CAU subjects. Pathway study revealed that "Communication between innate and adaptive immune cells"/"Primary immunodeficiency signaling" are significantly down-regulated in AA patients and "Interferon signaling"/"Complement System" are significantly down-regulated in CAU patients.
These newly identified genetic markers in WBCs provide valuable information about the pathophysiology of T2D and can be used for diagnosis and pharmaceutical drug design. Our results also found that AA and CAU patients with T2D express genes and pathways differently.