Prognostic value of plasma levels of secretory type II phospholipase A2 in patients with unstable angina pectoris

Kugiyama, Kiyotaka; Ota, Yasutaka; Sugiyama, Seigo; Kawano, Hiroaki; Doi, Hideki; Soejima, Hirofumi; Miyamoto, Shinzo; Ogawa, Hisao; Takazoe, Keiji; Yasue, Hirofumi

doi:10.1016/s0002-9149(00)01069-9

Cited by 74 publications

(51 citation statements)

References 20 publications

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“…Pla2g2a, which encodes the Pla2 group II A secreted phospholipase A2, showed an over 40-fold lower expression in whole blood after the injection of rAAV2/1-CMV-GH1 than in the NC controls (p < 0.05). Pla2g2a plays diverse roles in human diseases, including colon cancer, coronary artery disease and inflammation [17][18][19][20][21]. The mRNA expression of Gpr109a showed an over 10-fold increase in rat whole blood samples after the injection of rAAV2/1-CMV-GH1 (p < 0.05).…”

Section: Discussionmentioning

confidence: 98%

A microarray gene analysis of peripheral whole blood in normal adult male rats after long-term GH gene therapy

Qin

Tian

2010

Cellular and Molecular Biology Letters

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The main aims of this study were to determine the effects of GH gene abuse/misuse in normal animals and to discover genes that could be used as candidate biomarkers for the detection of GH gene therapy abuse/misuse in humans. We determined the global gene expression profile of peripheral whole blood from normal adult male rats after long-term GH gene therapy using CapitalBio 27 K Rat Genome Oligo Arrays. Sixty one genes were found to be differentially expressed in GH gene-treated rats 24 weeks after receiving GH gene therapy, at a two-fold higher or lower level compared to the empty vector group (p < 0.05). These genes were mainly associated with angiogenesis, oncogenesis, apoptosis, immune networks, signaling pathways, general metabolism, type I diabetes mellitus, carbon fixation, cell adhesion molecules, and cytokine-cytokine receptor interaction. The results imply that exogenous GH gene expression in normal subjects is likely to induce cellular changes in the metabolism, signal pathways and immunity. A real-time qRT-PCR analysis of a selection of the genes confirmed the microarray data. Eight differently expressed genes were selected as candidate biomarkers from among these 61 genes. These 8 showed five-fold higher or lower expression levels after the GH gene transduction (p < 0.05). They were then validated in real-time PCR experiments using 15 single-treated blood samples and 10 control blood samples. In summary, we detected the gene expression profiles of rat peripheral whole blood after long-term GH gene therapy and screened eight genes as candidate biomarkers based on the microarray data. This will contribute to an increased mechanistic understanding of the effects of chronic GH gene therapy abuse/misuse in normal subjects.

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Section: Discussionmentioning

confidence: 98%

A microarray gene analysis of peripheral whole blood in normal adult male rats after long-term GH gene therapy

Qin

Tian

2010

Cellular and Molecular Biology Letters

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“…Furthermore, circulating levels of sPLA 2 , increased in various chronic inflammatory diseases, have been demonstrated to independently predict clinical coronary events in patients with unstable angina and documented coronary artery disease. 69,70 Matrix Metalloproteinase-9…”

Section: Szmitko Et Al Inflammation and Endothelial Cell Activation 2043mentioning

confidence: 99%

Biomarkers of Vascular Disease Linking Inflammation to Endothelial Activation

et al. 2003

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A therosclerosis is regarded as a dynamic and progressive disease arising from the combination of endothelial dysfunction and inflammation. [1][2][3][4][5][6] This article is the second in a 2-part series examining emerging markers of inflammation and endothelial cell activation. The first article 7 provided a brief overview of the link between inflammation, endothelial dysfunction, and atherosclerosis and began the examination of emerging inflammatory mediators. This second article continues with an exploration of more novel markers for cardiovascular disease.

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“…The cascade of Lp-PLA2 activity may eventually lead to plaque destabilization, increasing the possibility of rupture and thrombosis (Hsieh et al, 2000). Confirming the same, circulating levels of sPLA2 were found to increase not only in various chronic inflammatory diseases but also independently predicted clinical coronary events in patients with unstable angina and documented coronary artery disease (Kugiyama et al, 1999(Kugiyama et al, , 2000.…”

Section: Lipoprotein-associated Phospholipase A-2 (Lp-pla-2)mentioning

confidence: 73%