Transcriptome alterations of mitochondrial and coagulation function in schizophrenia by cortical sequencing analysis — ASN Events
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Transcriptome alterations of mitochondrial and coagulation function in schizophrenia by cortical sequencing analysis (#87)

Kuo-Chuan Huang 1 , Ko-Chun Yang 2 , Han Lin 2 , Theresa Tsun-Hui Tsao 3 , Sheng-An Lee 4
  1. Department of Psychiatry, Beitou Branch, Tri-Service General Hospital, Taipei, Taiwan
  2. Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan
  3. Department of Biochemical Science and Technology,, National Taiwan University, Taipei, Taiwan
  4. Department of Information Management, Kainan University, Taoyuan, Taiwan

Background

Genetic and protein interactions in schizophrenia may predispose to biological dysfunction of energy metabolism and hemostasis. A comparison of schizophrenic candidate genes from literature reviews was explored. The differential expression level of schizophrenic candidate genes from NGS BA22 brain samples and associated mediator genes constructed schizophrenia-mediator network(SCZMN). The corresponding pathways searched against pathway databases such as PID, Reactome, HumanCyc, and Cell-Map and the candidate complexes by CORUM were identified by MCL clustering for potential pathogenesis of schizophrenia.

Results

We identified genes which were over- or under-expressed in the BA22 brain samples of schizophrenia and proposed them as schizophrenia candidate marker genes(SCZCGs). The genetic interactions of mitochondrial genes surrounded by most under-expressed SCZCGs indicates the genetic predisposition of mitochondria dysfunction in schizophrenia. The biological functions of SCZCGs, as listed in the Pathway Interaction Database (PID), indicate that these genes have roles in DNA binding transcription factor, signal and cancer-related pathways, coagulation and cell cycle regulation and differentiation pathways. The relationship between antipsychotic target genes (DRD2/3 and HTR2A) and coagulation factor genes (F3, F7 and F10) appeared to cascade the following hemostatic process implicating the bottleneck of coagulation genetic network by the bridging of actin-binding protein (FLNA).

Conclusions

Transcriptome sequencing of brain specific samples provides enrichment analysis of differential expression and genetic interaction in evaluation of mitochondrial and coagulation function in schizophrenia. Energy metabolism and hemostatic process have important roles in the pathogenesis for schizophrenia.