Gene and expression analyses reveal enhanced expression of pericentrin 2 (PCNT2) in bipolar disorder.
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.
Anitha
Ayyappan
A
Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Nakamura
Kazuhiko
K
Yamada
Kazuo
K
Iwayama
Yoshimi
Y
Toyota
Tomoko
T
Takei
Nori
N
Iwata
Yasuhide
Y
Suzuki
Katsuaki
K
Sekine
Yoshimoto
Y
Matsuzaki
Hideo
H
Kawai
Masayoshi
M
Miyoshi
Ko
K
Katayama
Taiichi
T
Matsuzaki
Shinsuke
S
Baba
Kousuke
K
Honda
Akiko
A
Hattori
Tsuyoshi
T
Shimizu
Shoko
S
Kumamoto
Natsuko
N
Tohyama
Masaya
M
Yoshikawa
Takeo
T
Mori
Norio
N
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
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