title: Gene and expression analyses reveal enhanced expression of pericentrin 2 (PCNT2) in bipolar disorder.
abstract: BACKGROUND
  DISC1 has been suggested as a causative gene for psychoses in a large Scottish kindred. PCNT2 has recently been identified as an interacting partner of DISC1. In this study, we investigated the role of PCNT2 in bipolar disorder, by gene expression analysis and genetic association study.
  
  
  METHODS
  By TaqMan real-time quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), we examined the messenger RNA (mRNA) levels of PCNT2 in the postmortem prefrontal cortex of bipolar disorder (n = 34), schizophrenia (n = 31), and control subjects (n = 32), obtained from Stanley Array Collection. We also compared the mRNA levels of PCNT2 in the peripheral blood lymphocytes of bipolar disorder (n = 21), schizophrenia (n = 21), depression (n = 33), and control subjects (n = 57). For the association study, 23 single nucleotide polymorphisms (SNPs) were analyzed in 285 bipolar disorder patients and 287 age-and gender-matched control subjects, all of Japanese origin. The genotypes were determined by TaqMan assay.
  
  
  RESULTS
  Significantly higher expression of PCNT2 was observed in the brain samples of bipolar group, compared with the control (p = .001) and schizophrenia (p = .018) groups. In the peripheral blood lymphocytes also, a significantly higher expression of PCNT2 was observed in the bipolar group, compared with the control subjects (p = .043). However, none of the SNPs analyzed in our study showed a significant association with bipolar disorder; a weak tendency toward association was observed for two intronic SNPs.
  
  
  CONCLUSIONS
  Our findings suggest that elevated levels of PCNT2 might be implicated in the pathophysiology of bipolar disorder.
authors: Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
authors: Ayyappan
authors: A
authors: Anitha
authors: Kazuhiko
authors: K
authors: Nakamura
authors: Kazuo
authors: K
authors: Yamada
authors: Yoshimi
authors: Y
authors: Iwayama
authors: Tomoko
authors: T
authors: Toyota
authors: Nori
authors: N
authors: Takei
authors: Yasuhide
authors: Y
authors: Iwata
authors: Katsuaki
authors: K
authors: Suzuki
authors: Yoshimoto
authors: Y
authors: Sekine
authors: Hideo
authors: H
authors: Matsuzaki
authors: Masayoshi
authors: M
authors: Kawai
authors: Ko
authors: K
authors: Miyoshi
authors: Taiichi
authors: T
authors: Katayama
authors: Shinsuke
authors: S
authors: Matsuzaki
authors: Kousuke
authors: K
authors: Baba
authors: Akiko
authors: A
authors: Honda
authors: Tsuyoshi
authors: T
authors: Hattori
authors: Shoko
authors: S
authors: Shimizu
authors: Natsuko
authors: N
authors: Kumamoto
authors: Masaya
authors: M
authors: Tohyama
authors: Takeo
authors: T
authors: Yoshikawa
authors: Norio
authors: N
authors: Mori
mesh_terms: D000328:Adult; D000941:Antigens / Q000235:genetics* / Q000378:metabolism; D001665:Binding Sites; D001714:Bipolar Disorder / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D002891:Chromosomes, Human, Pair 21 / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D005260:Female; D015870:Gene Expression / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D017397:Prefrontal Cortex / Q000378:metabolism; D012313:RNA / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D000941:Antigens; C412476:DISC1 protein, human; D004268:DNA-Binding Proteins; C118711:LZTS1 protein, human; D009419:Nerve Tissue Proteins; D025521:Tumor Suppressor Proteins; C086178:pericentrin; D012313:RNA