Myeloperoxidase genetic polymorphisms and susceptibility to Kawasaki disease in Taiwanese children

Weng, Ken‐Pen; Hsieh, Kai‐Sheng; Huang, Shih-Hui; Wu, Huang-Wei; Chien, Jen-Hung; Lin, Chu-Chuan; Tang, Chia-Wan; Ou, Shan-Fu; Huang, Sin-Jhih; Ger, Luo‐Ping

doi:10.1016/j.jmii.2015.05.004

Cited by 4 publications

(5 citation statements)

References 29 publications

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“…The findings of numerous different studies have shown that several factors induce the formation of CRC, included genetic and epigenetic alterations (28,29). Some of these gene alterations can be applied as biomarkers for cancer diagnosis and provide strategies for cancer therapy (30). The human ANP32A gene is expressed differently in different tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer

et al. 2017

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Acidic leucine-rich nuclear phosphoprotein-32A (ANP32A) possesses multiple biochemical activities, has been found to be decreased or absent in malignant tumors. However, new findings have shown that it is expressed in greater amounts in advanced cancers than in early-stage tumors. The role and clinical significance of ANP32A in colorectal cancer (CRC) is still unknown. In the present study, the expression of ANP32A was assessed in 68 CRC patients by IHC, and then the correlation of its expression with clinicopathological factors was investigated using the Allred, Klein and immune response scoring system analysis. Western blot and real-time PCR analyses were used to assess ANP32A expression and the activity of Akt and p38 in cancer and normal tissues. These data indicated a significant association between ANP32A expression and the activity of Akt and p38, besides the tumor differentiation status in CRC patients. IHC and western blotting data revealed that ANP32A was overexpressed in CRC patients, and ANP32A levels were higher in poorly differentiated tumors. Protein and mRNA analysis revealed that with a high expression of ANP32A, the activation of Akt was enhanced, while the p-38 phosphorylation level was decreased in CRC tissues. MTT assay and functional studies revealed that knockdown of ANP32A inhibited cell growth and induced p38 phosphorylation and Akt dephosphorylation. The present study indicated that ANP32A promoted CRC proliferation by inhibition of p38 and activation of Akt signaling pathways and suggested that ANP32A may play a potential role in CRC diagnosis and therapy.

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Section: Discussionmentioning

confidence: 99%

ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer

et al. 2017

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“…However, high levels of MPO correlate with the prevalence of certain autoimmune diseases. Downregulation of MPO expression has been associated with incidence and se-verity of lupus erythematodes [38], Kawasaki's disease [39], inflammatory bowel disease [40] and eosinophilic granulomatosis [41]. About half of the patients with eosinophilic granulomatosis showed perinuclear anti-neutrophil cytoplasmatic antibodies (pANCA) directed against MPO.…”

Section: Introduction Mpo Conservation Across Species Maturation In Myeloid Progenitors and Its Role In Immune Responsesmentioning

confidence: 99%

The Enzymatic and Non-Enzymatic Function of Myeloperoxidase (MPO) in Inflammatory Communication

et al. 2021

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Myeloperoxidase is a signature enzyme of polymorphonuclear neutrophils in mice and humans. Being a component of circulating white blood cells, myeloperoxidase plays multiple roles in various organs and tissues and facilitates their crosstalk. Here, we describe the current knowledge on the tissue- and lineage-specific expression of myeloperoxidase, its well-studied enzymatic activity and incoherently understood non-enzymatic role in various cell types and tissues. Further, we elaborate on Myeloperoxidase (MPO) in the complex context of cardiovascular disease, innate and autoimmune response, development and progression of cancer and neurodegenerative diseases.

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“…21 Studies of MPO polymorphisms have mainly concentrated on the -463G>A polymorphism (GenBank ID: rs2333227), and a recent case-control study suggested that the G allele of this polymorphism may be a possible genetic risk factor for KD. [22][23][24] Additionally, SLC11A1 can modulate the interactions between macrophages and interferon-c derived from bacterial lipopolysaccharide and/or natural killer cells or T cells. 24 A previous study demonstrated that allele 1 of the 5' promoter (GT)n repeat in the SLC11A1 gene was related to KD.…”

Section: Discussionmentioning

confidence: 99%

“…[22][23][24] Additionally, SLC11A1 can modulate the interactions between macrophages and interferon-c derived from bacterial lipopolysaccharide and/or natural killer cells or T cells. 24 A previous study demonstrated that allele 1 of the 5' promoter (GT)n repeat in the SLC11A1 gene was related to KD. 25 MMP9 has been implicated in various pathological situations, including tumor metastasis, KD, inflammation, and atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential core genes in Kawasaki disease using bioinformatics analysis

You

Zhong

et al. 2019

J Int Med Res

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Objective The present study aimed to elucidate the underlying pathogenesis of Kawasaki disease (KD) and to identify potential biomarkers for KD. Methods Gene expression profiles for the GSE68004 dataset were downloaded from the Gene Expression Omnibus database. The pathways and functional annotations of differentially expressed genes (DEGs) in KD were examined by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses using the Database for Annotation, Visualization and Integrated Discovery (DAVID) tool. Protein–protein interactions of the above-described DEGs were investigated using the Search Tool for the Retrieval of Interacting Genes (STRING). Results Gene Ontology analysis revealed that DEGs in KD were significantly enriched in biological processes, including the inflammatory response, innate immune response, defense response to Gram-positive bacteria, and antibacterial humoral response. In addition, 10 hub genes with high connectivity were selected from among these DEGs ( ITGAM, MPO, MAPK14, SLC11A1, HIST2H2BE, ELANE, CAMP, MMP9, NTS, and HIST2H2AC). Conclusion The identification of several novel hub genes in KD enhances our understanding of the molecular mechanisms underlying the progression of this disease. These genes may be potential diagnostic biomarkers and/or therapeutic molecular targets in patients with KD. ITGAM inhibitors in particular may be potential targets for KD therapy.

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Myeloperoxidase genetic polymorphisms and susceptibility to Kawasaki disease in Taiwanese children

Abstract: Our results suggest that G allele of MPO -463G>A polymorphism is a potential genetic marker for KD risk in Taiwanese children.

Cited by 4 publications

References 29 publications

ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer

ANP32A modulates cell growth by regulating p38 and Akt activity in colorectal cancer

The Enzymatic and Non-Enzymatic Function of Myeloperoxidase (MPO) in Inflammatory Communication

Identification of potential core genes in Kawasaki disease using bioinformatics analysis

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