ArticleThe international journal of neuropsychopharmacology2014
Reduced mRNA expression of PTGDS in peripheral blood mononuclear cells of rapid-cycling bipolar disorder patients compared with healthy control subjects.
Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- PTGDS: As a Specific Biomarker for Septic Cardiomyopathy.Infection and drug resistance · 2025Article
- Dietary resveratrol and β-Hydroxy-β-Methylbutyric acid enhance flavor and modulate intramuscular fat in Tibetan sheep: insights from transcriptomics and lipidomics.Frontiers in veterinary science · 2025Article
- Article
- Lipid Biomarker Research in Bipolar Disorder: A Scoping Review of Trends, Challenges, and Future Directions.Biological psychiatry global open science · 2023Article
- SNX10 and PTGDS are associated with the progression and prognosis of cervical squamous cell carcinoma.BMC cancer · 2021Article
- Update on the human and mouse lipocalin (LCN) gene family, including evidence the mouse Mup cluster is result of an "evolutionary bloom".Human genomics · 2019Review
- Exon Array Biomarkers for the Differential Diagnosis of Schizophrenia and Bipolar Disorder.Molecular neuropsychiatry · 2018Article
- Blood Gene Expression Profile Predicts Response to Antipsychotics.Frontiers in molecular neuroscience · 2018Article
- A Genome-Wide Association Study and Complex Network Identify Four Core Hub Genes in Bipolar Disorder.International journal of molecular sciences · 2017Article
- Observational
- Understanding epigenetic architecture of suicide neurobiology: A critical perspective.Neuroscience and biobehavioral reviews · 2017Review
- A composite peripheral blood gene expression measure as a potential diagnostic biomarker in bipolar disorder.Translational psychiatry · 2015Article
- Shortened telomere length in bipolar disorder: a comparison of the early and late stages of disease.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999)Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDisturbances related to the arachidonic acid cascade and prostaglandin metabolism may be involved in the pathophysiology of bipolar disorder, as supported by a recent genome-wide association study meta-analysis; however, evidence from clinical studies on a transcriptional level is lacking. Two enzymes in the arachidonic acid cascade are the prostaglandin D synthase (PTGDS), which catalyzes the conversion of prostaglandin H2 to prostaglandin D2 (PGD2), and the aldo-keto reductase family 1 member C3 (AKR1C3), which catalyzes the reduction of PGD2. We aimed to test the hypothesis that mRNA expression of PTGDS and AKR1C3 is deregulated in rapid-cycling disorder patients in a euthymic or current affective state compared with healthy control subjects, and that expression alters with affective states.
methodsPTGDS and AKR1C3 mRNA expression in peripheral blood mononuclear cells was measured in 37 rapid-cycling bipolar disorder patients and 40 age- and gender-matched healthy control subjects using reverse transcription quantitative real-time polymerase chain reaction. Repeated measurements of PTGDS and AKR1C3 mRNA expression were obtained in various affective states during 6-12 months and compared with repeated measurements in healthy control subjects.
resultsAdjusted for age and gender, PTGDS mRNA expression was down-regulated in rapid-cycling bipolar disorder patients in a euthymic, depressive, and manic/hypomanic state compared with healthy control subjects. No difference in PTGDS mRNA expression was observed between affective states. AKR1C3 mRNA expression did not differ between bipolar disorder patients in any affective state or in comparison with healthy control subjects.
conclusionsThe results suggest a role for aberrantly-regulated PTGDS mRNA expression in rapid-cycling bipolar disorder. The sample size was limited; replication of the findings in larger, independent samples is warranted to further explore the role of the arachidonic acid cascade and prostaglandin metabolism as a potential therapeutic target in bipolar disorder.
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