Abstract
Keshan disease (KD) is a kind of endemic cardiomyopathy which has a high mortality. However, molecular mechanism in the pathogenesis of KD remains poorly understood. Serum samples were collected from 112 KD patients and 112 normal controls. Gene microarray was used to screen differently expressed genes. Genevestigator was applied to forecast co-expression genes of significant gene. iTRAQ proteomics analysis was used to verify significant genes and their co-expression genes. GO, COG, IPA and STRING were applied to undertake function categorization, pathway and network analysis separately. We identified 32 differentially expressed genes; IDH2, FEM1A, SSPB1 and their respective 30 co-expression genes; 68 differential proteins in KD. Significant proteins were categorized into 23 biological processes, 16 molecular functions, 16 cellular components, 15 function classes, 13 KD pathways and 1 network. IDH2, FEM1A, SSBP1, CALR, NDUFS2, IDH3A, GAPDH, TCA Cycle II (Eukaryotic) pathway and NADP repair pathway may play important roles in the pathogenesis of KD.
Highlights
Keshan disease (KD) is a kind of endemic cardiomyopathy which has a high mortality
The analysis of microarray data using the fold change criteria ≥3 and ≤0.33, revealed 32 up-regulated genes in KD compared to normal controls were noticed (Table 1)
To confirm the differential expression of the genes revealed by microarray analysis, the genes of IDH2, fem-1 homolog A (FEM1A) and single stranded DNA binding protein 1 (SSBP1), which had different magnitudes of fold changes of gene expression, were selected for the assessment by quantitative reverse transcription-polymerase chain reaction (qRT-PCR)
Summary
Keshan disease (KD) is a kind of endemic cardiomyopathy which has a high mortality It was reported firstly in Keshan County in northeast China in 1935, while the similar cases were found in Nagano Prefecture in Japan and northern mountains in North Korea in the 1950s1. The levels of selenium in the blood and hair of the patients with KD are significantly lower than those in the normal control individuals[3]. The different expression genes between the KD patients and normal controls were screened by our whole-genome microarray analysis[4]. Nine different expression protein spots were observed between Keshan disease patients and health control ones in 2-dimensional gel electrophoresis images, of which eight were identified by MALDI-TOF-MS6. Gene name TTC25 RMND5A IDH2 A2ML1 FBXO15 ZDHHC2 LEF1 FEM1A CD3G SSBP1 RASD1 SIGLEC8 ABCC13 DIO3 PDE8B TNFSF11 TNNT2 THBS1 ABI3BP MGAT3 EYA4 SEZ6L2 NUCKS1 IGF2BP2 KRR1 GUCD1 ACSL6 C18orf[10] REXO2 MYBPC3 EFNA1 CYP2B6
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