Down-regulation of PRKCB1 expression in Han Chinese patients with subsyndromal symptomatic depression |
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| Affiliation: | 1. College of Pharmacy, Ajou University, 206, Worldcup-ro, Yeongtong-gu, Suwon 443-749, Republic of Korea;2. Research Institute of Pharmaceutical Sciences and Technology, Ajou University, 206, Worldcup-ro, Yeongtong-gu, Suwon 443-749, Republic of Korea;3. Department of Pharmacology, Yonsei University, College of Medicine, 50, Yonsei-ro, Seodaemun-gu, Seoul 120-752, Republic of Korea;1. Department of Pathophysiology, Key Laboratory of Ministry of Education of China for Neurological Disorders, School of Basic Medicine of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;2. Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, No.8, Longyuan Road, Nanshan District, Shenzhen 518055, China;3. Department of Laboratory Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China;4. Co-innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China;1. Department of Psychological Medicine, Zhongshan Hospital, Fudan University, Shanghai 200032, China;2. Department of Psychiatry, Tongji Hospital of Tongji University, Shanghai 200065, China;3. Department of Neurology, Zhongshan Hospital, Fudan University, Shanghai 200032, China |
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| Abstract: | BackgroundSubsyndromal symptomatic depression (SSD) is a common disease with significant social dysfunction. However, SSD is still not well understood and the pathophysiology of it remains unclear.MethodsWe classified 48 candidate genes for SSD according to our previous study into clusters and pathways using DAVID Bioinformatics Functional Annotation Tool. We further replicated the result by using real-time Quantitative PCR (qPCR) studies to examine the expression of identified genes (i.e., STAT5b, PKCB1, ABL1 and NRAS) in another group of Han Chinese patients with SSD (n = 50). We further validated the result by examining PRKCB1 expression collected from MDD patients (n = 20). To test whether a deficit in PRKCB1 expression leads to dysregulation in PRKCB1 dependent transcript networks, we tested mRNA expression levels for the remaining 44 genes out of 48 genes in SSD patients. Finally, the power of discovery was improved by incorporating information from Quantitative Trait (eQTL) analysis.ResultsThe results showed that the PRCKB1 gene expression in peripheral blood mononuclear cells (PBMC) was 33.3% down-regulated in SSD patients (n = 48, t = 3.202, p = 0.002), and a more dramatic (n = 17, 49%) down-regulation in MDD patients than control (n = 49, t = 2.114, p = 0.001). We also identified 37 genes that displayed a strong correlation with PRKCB1 mRNA expression levels in SSD patients. The expression of PRKCB1 was regulated by multiple single nucleotide polymorphisms (SNPs) both at the transcript level and exon level.ConclusionsIn conclusion, we first found a significant decrease of PRCKB1 mRNA expression in SSD, suggesting PRKCB1 might be the candidate gene and biomarker for SSD. |
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| Keywords: | Subsyndromal symptomatic depression Major depressive disorder ERBB signal pathway Gene expression |
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