The expression of genes encoding for COX-2, MPO, iNOS, and sPLA2-IIA in patients with recurrent depressive disorder

Gałecki, Piotr; Gałecka, Elżbieta; Maes, Michaël; Chamielec, Marcelina; Orzechowska, Agata; Bobińska, Kinga; Lewiński, Andrzej; Szemraj, Janusz

doi:10.1016/j.jad.2012.01.016

Cited by 131 publications

(87 citation statements)

References 71 publications

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“…For example, we found that allele of the functional polymorphic variant of the COX-2 and MPO gene, that are related to the higher expression, are both a risk factor for depression (Ga"ecki et al, 2010a, b). Moreover, we found that the gene expression of the enzyme is increased in the disease in question (Ga"ecki et al, 2012). Nevertheless, gene and protein expression are under the regulation of many post-transcriptional and posttranslational mechanisms.…”

Section: Discussionmentioning

confidence: 85%

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Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Gałecki

Orzechowska

Berent

et al. 2013

Journal of Affective Disorders

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Section: Discussionmentioning

confidence: 85%

“…For example, bacterial and viral infectious where ''sickness behavior'' is a common denominator (Maes et al, 2012). The appearance of depressive symptoms can also often be observed in rheumatoid arthritis or asthma and other inflammatory diseases (Covic et al, 2012;Trzciń ska et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Gałecki

Orzechowska

Berent

et al. 2013

Journal of Affective Disorders

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“…It has been known that disruption of the mouse PLA2G2A, a potential source of AA for COX-2, increases tumor number despite the fact that the mutation has been predicted to decrease prostaglandin production (Hong KH, et al, 2001). Some studies have suggested that PLA2G2A and COX-2 play a role in other diseases (Galecki et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Phospholipase A₂Group IIA in Esophageal Squamous Cell Carcinoma and Association with Cyclooxygenase-2 Expression

Zhai¹,

Dong²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Asian Pac J Cancer Prev, 15 (21), 9417-9421 IntroductionEsophageal cancer is a highly aggressive malignant disease with a 5-year survival rate of 10% to 15% (Ferri et al., 2012). The incidence of esophageal cancer varies greatly between populations and across geographic regions. The Taihangshan Mountain area, including Linxian in Henan Province, a rural area of China, has the highest incidence of esophageal cancer, especially squamous cell carcinoma (ESCC), in the world (>100 per 100, 000 population) (Zhang et al., 2011;Lin et al., 2013).Inflammation has been recognized as a contributing factor for the pathogenesis of ESCC. There are results showing that two key inflammatory enzymes, Phospholipase A 2 Group IIA (PLA2G2A) and cyclooxygenase-2 (COX-2) are involved in the pathways of arachidonic acid (AA) biosynthesis, and both play an important role in inflammation and angiogenesis as well as cancer (Murakami et al., 2011). Recently, we reported that PLA2G2A and COX-2 gene single nucleotide polymorphisms (SNPs) may modify the risk of ESCC

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“…A first example is COX-2 inhibition. Trials with selective COX-2 inhibitors in depression were initiated before it was known that COX-2 expression is increased in depression and thus that COX-2 is a new possible drug target in depression [61,62]. It was known that selective COX-2 inhibitors may cause neuro-inflammation, aggravate Th1 responses, decrease the levels of key antioxidants, increase lipid peroxidation, cause bacterial translocation, damage mitochondria, and aggravate neuroprogression and cardiovascular disorder [61].…”

Section: Gaps and Required Improvements: New Treatmentsmentioning

confidence: 99%

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

et al. 2015

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Meta-analyses confirm that depression is accompanied by signs of inflammation including increased levels of acute phase proteins, e.g. C-reactive protein, and pro-inflammatory cytokines, e.g. interleukin-6. Supporting the translational significance of this, a meta-analysis showed that anti-inflammatory drugs may have antidepressant effects. Here we argue that inflammation and depression research needs to get onto a new track. Firstly, the choice of inflammatory biomarkers in depression research was often too selective and did not consider the broader pathways.Secondly, although mild inflammatory responses are present in depression, other immune-related pathways cannot be disregarded as new drug targets, e.g. activation of cell-mediated immunity, oxidative and nitrosative stress (O&NS) pathways, autoimmune responses, bacterial translocation, activation of the Toll-like Receptor and neuroprogressive pathways. Thirdly, antiinflammatory treatments are sometimes used without full understanding of their effects on the broader pathways underpinning depression. Since many of the activated immune-inflammatory pathways in depression actually confer protection against an overzealous inflammatory response, targeting these pathways may result in unpredictable and unwanted results. Furthermore, this paper discusses the required improvements in research strategy, i.e. path and drug discovery processes, omics-based techniques and systems biomedicine methodologies. Firstly, novel methods should be employed to examine the intracellular networks that control and modulate the immune, O&NS and neuroprogressive pathways using omics-based assays, including genomics, transcriptomics, proteomics, metabolomics, epigenomics and microbiomics. Secondly, systems biomedicine analyses are essential to unravel the complex interactions between these cellular 4 networks, pathways and the multifactorial trigger factors and to delineate new drug targets in the cellular networks or pathways. Drug discovery processes should delineate new drugs targeting the intracellular networks and immune-related pathways.

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The expression of genes encoding for COX-2, MPO, iNOS, and sPLA2-IIA in patients with recurrent depressive disorder

Cited by 131 publications

References 71 publications

Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Overexpression of Phospholipase A₂Group IIA in Esophageal Squamous Cell Carcinoma and Association with Cyclooxygenase-2 Expression

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

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The expression of genes encoding for COX-2, MPO, iNOS, and sPLA2-IIA in patients with recurrent depressive disorder

Cited by 131 publications

References 71 publications

Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Vascular endothelial growth factor receptor 2 gene (KDR) polymorphisms and expression levels in depressive disorder

Overexpression of Phospholipase A2Group IIA in Esophageal Squamous Cell Carcinoma and Association with Cyclooxygenase-2 Expression

Toward Omics-Based, Systems Biomedicine, and Path and Drug Discovery Methodologies for Depression-Inflammation Research

Contact Info

Product

Resources

About

Overexpression of Phospholipase A₂Group IIA in Esophageal Squamous Cell Carcinoma and Association with Cyclooxygenase-2 Expression