Methylation status of the reelin promoter region in the brain of schizophrenic patients.

Abstract

BACKGROUND:

Hypermethylation of the reelin (RELN) promoter region and the reduced levels of its messenger RNA and protein have been implicated in the pathophysiology of schizophrenia. We intended a technical replication of recent studies that observed hypermethylation of CpG or CpNpG sites in the RELN promoter region in the brain of schizophrenic patients.

METHODS:

The DNA methylation status of the promoter region of RELN was examined by using the pyrosequencing method in the prefrontal cortices of 14 patients with schizophrenia and 13 control subjects.

RESULTS:

All of the CpG and two proposed CpNpG sites analyzed showed no detectable DNA methylation (< 5%) in both control subjects and patients with schizophrenia. No detectable DNA methylation was observed in both gray and white matter, excluding the possibility of cellular heterogeneity of start materials.

CONCLUSIONS:

We did not confirm the hypermethylation of the RELN promoter region in the brains of schizophrenic patients, suggested in the previous studies.

• Authors: Mamoru Tochigi, Kazuya Iwamoto, Miki Bundo, Atsuko Komori, Tsukasa Sasaki, Nobumasa Kato, Tadafumi Kato
• Journal: Biological psychiatry (Biol Psychiatry) Vol. 63 Issue 5 Pg. 530-3 (Mar 01 2008) ISSN: 1873-2402 [Electronic] United States
• PMID: 17870056 (Publication Type: Journal Article)

Chemical References

• Cell Adhesion Molecules, Neuronal
• Extracellular Matrix Proteins
• Nerve Tissue Proteins
• RNA, Messenger
• Reelin Protein
• RELN protein, human
• Serine Endopeptidases

Topics

• Cell Adhesion Molecules, Neuronal (genetics)
• DNA Methylation
• Epigenesis, Genetic (genetics)
• Extracellular Matrix Proteins (genetics)
• Humans
• Nerve Tissue Proteins (genetics)
• Polymerase Chain Reaction
• Prefrontal Cortex (pathology)
• Promoter Regions, Genetic (genetics)
• RNA, Messenger (genetics)
• Reelin Protein
• Schizophrenia (genetics, pathology)
• Sequence Analysis, DNA
• Serine Endopeptidases (genetics)