Expression in normals and in subjects with schizophrenia of a novel gene fragment originally isolated from monozygotic twins discordant for schizophrenia

Abstract

Differentially expressed clones from subtracted cDNA libraries of a pair of monozygotic twins discordant for schizophrenia have been reported in the literature. The clones were expressed in lymphocytes from the healthy twin, but not from the schizophrenic twin. In the current study, we assessed the expression of one of these clones, oksc12b, in 10 normal controls and in 10 patients who met DSM-IV criteria for schizophrenia and had never received neuroleptic medication. We hypothesized that this clone would be differentially expressed in normal controls and in the schizophrenic patients, and that its expression could be a peripheral marker of the disease. Lymphocytes were isolated and total RNA was purified, reverse-transcribed, and quantified by two PCR methods. In the first PCR assay, oksc12b expression was measured relative to beta-actin gene expression. The second PCR assay consisted of a competitive procedure using a heterologous DNA internal standard. Neither method confirmed any difference in oksc12b expression between schizophrenic patients and normal controls. Subtypes of schizophrenia or the general heterogeneity of this syndrome may explain the discrepancy found. It is also possible that the differentially expressed clones are present in discordant monozygotic twins, but not in other patients.

Spermatozoal cell death-inducing DNA fragmentation factor-α-like effector A (CIDEA) gene expression and DNA fragmentation in infertile men with metabolic syndrome and normal seminogram

“…The mRNA of β-actin was used as an endogenous external control for RT-PCR: Primers for β-actin to generate a (218 bp) fragment were designed as sense primers, 5′-AAGAGAGGCATCCTCACCCT-3′ and antisense primers, 5′-TACATGGCTGGGGTGTTGAA-3′ [22]. …”

Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives

“…It produces various reactive byproducts such as superoxide radical and H 2 O 2 [16,17]. Moreover, in mammals, a range of protein complexes also produce ROS, such as Nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R) [18], dihydroorotate dehydrogenase (DHODH) [19,20], complex II: succinate dehydrogenase (SDH) [21,22], and monoamine oxidases (MAO) [23]. Several defense systems, in the form of antioxidants like GPXs, TRXPs, SODs, PRDXs, GSH, TRX2, GRX2, cyt c oxidase (complex IV), coenzyme Q, ascorbic acid, vitamin E and carotenes, protect the mitochondria from detrimental effects of ROS [23][24][25][26].…”

Genetic or epigenetic difference causing discordance between monozygotic twins as a clue to molecular basis of mental disorders

“…However, the expression level of this gene in the brains of patients with schizophrenia did not differ from controls, suggesting no pathophysiological significance. 71 Summary of the findings: In summary, difference of DNA sequence has been searched for in MZ twins discordant for schizophrenia, but most of the studies did not support the genetic difference. The results in the difference in DNA methylation seem a little more promising.…”