Dataset Information

PPARD May Play a Protective Role against the Development of Schizophrenia.

ABSTRACT: PPARD has been suggested to contribute to the etiology of schizophrenia (SCZ) with the underlying mechanisms largely unknown. Here, we first collected and analyzed the PPARD expression profile from three groups: (1) 18 healthy control (HC) subjects, (2) 14 clinical high-risk (CHR) patients, and (3) 19 early onset of SCZ (EOS) patients. After that, we conducted a systematical pathway analysis to explore the potential mechanisms involved in PPARD exerting influence on the pathological development of SCZ. Compared to the HC group, the expression of PPARD was slightly decreased in the EOS group (LFC = -0.34; p = 0.23) and increased in the CHR group (LFC = 0.65; p = 0.20). However, there was a significant difference between the EOS group and the CHR group (LFC = -0.99; p = 0.015), reflecting the amount of variation in PPARD expression before and after the onset of SCZ. Pathway analysis suggested that overexpression of PPARD may regulate ten proteins or molecules to inhibit the pathological development of SCZ, including the deactivation of eight SCZ promoters and stimulation of two SCZ inhibitors. Our results support the association between PPARD and SCZ. The pathways identified may help in the understanding of the potential mechanisms by which PPARD contributes to the etiology of SCZ.

SUBMITTER: Li X

PROVIDER: S-EPMC7428834 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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PPARD May Play a Protective Role against the Development of Schizophrenia.

Li Xinrong X Liu Sha S Kapoor Karan K Xu Yong Y

PPAR research 20200807

PPARD has been suggested to contribute to the etiology of schizophrenia (SCZ) with the underlying mechanisms largely unknown. Here, we first collected and analyzed the PPARD expression profile from three groups: (1) 18 healthy control (HC) subjects, (2) 14 clinical high-risk (CHR) patients, and (3) 19 early onset of SCZ (EOS) patients. After that, we conducted a systematical pathway analysis to explore the potential mechanisms involved in PPARD exerting influence on the pathological development ...[more]

PMID: 32831816

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Project description:BackgroundOsteoarthritis (OA) is the most prevalent form of arthritis and the major cause of disability and overall diminution of quality of life in the elderly population. Currently there is no cure for OA, partly due to the large gaps in our understanding of its underlying molecular and cellular mechanisms. Macrophage migration inhibitory factor (MIF) is a procytokine that mediates pleiotropic inflammatory effects in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, data on the role of MIF in OA is limited with conflicting results. We undertook this study to investigate the role of MIF in OA by examining MIF genotype, mRNA expression, and protein levels in the Newfoundland Osteoarthritis Study.MethodsOne hundred nineteen end-stage knee/hip OA patients, 16 RA patients, and 113 healthy controls were included in the study. Two polymorphisms in the MIF gene, rs755622, and -794 CATT5-8, were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR followed by automated capillary electrophoresis, respectively. MIF mRNA levels in articular cartilage and subchondral bone were measured by quantitative polymerase chain reaction. Plasma concentrations of MIF, tumor necrosis factor-alpha (TNF-?), interleukin-6 (IL-6), and interleukin-1 beta (IL-1?) were measured by enzyme-linked immunosorbent assay.Resultsrs755622 and -794 CATT5-8 genotypes were not associated with MIF mRNA or protein levels or OA (all p???0.19). MIF mRNA level in cartilage was lower in OA patients than in controls (p?=?0.028) and RA patients (p?=?0.004), while the levels in bone were comparable between OA patients and controls (p?=?0.165). MIF protein level in plasma was lower in OA patients than in controls (p?=?3.01?×?10-10), while the levels of TNF-?, IL-6 and IL-1? in plasma were all significantly higher in OA patients than in controls (all p???0.0007). Multivariable logistic regression showed lower MIF and higher IL-1? protein levels in plasma were independently associated with OA (OR per SD increase?=?0.10 and 8.08; 95% CI?=?0.04-0.19 and 4.42-16.82, respectively), but TNF-? and IL-6 became non-significant.ConclusionsReduced MIF mRNA and protein expression in OA patients suggested MIF might have a protective role in OA and could serve as a biomarker to differentiate OA from other joint disorders.

Dataset Information

PPARD May Play a Protective Role against the Development of Schizophrenia.

Publications

PPARD May Play a Protective Role against the Development of Schizophrenia.

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