Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

An infl ammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an infl ammatory protein produced at infl ammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and highsensitive C-reactive protein (hsCRP), another infl ammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the fi rst measurement, and between the change ratios (second value/fi rst value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the fi rst measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identifi ed PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r =-0.446, P = 0.006 versus r =-0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels

Plasma Pentraxin 3 is a More Potent Predictor of Endothelial Dysfunction than High-Sensitive C-Reactive Protein

An infl ammatory response is a key event for endothelial dysfunction. Pentraxin 3 (PTX3) is an infl ammatory protein produced at infl ammation sites such as leukocytes and vascular endothelial cells. Here, we compared the relationships between endothelial function assessed by flow-mediated dilation (FMD), and the levels of plasma PTX3 and highsensitive C-reactive protein (hsCRP), another infl ammatory protein of the pentraxin family. Levels of FMD, PTX3 and hsCRP were measured twice within 6 to 8 months and retrospectively analyzed in 36 patients with coronary artery disease. We examined the associations between the values of FMD and the levels of PTX3 and hsCRP at the fi rst measurement, and between the change ratios (second value/fi rst value) of these parameters. Univariate linear regression analysis showed significantly negative correlations between FMD values and PTX3 and hsCRP levels at the fi rst measurement, and significant associations with taking statins or calcium antagonists. Multivariate linear stepwise regression analysis identifi ed PTX3 levels and taking statins and calcium antagonists as independent factors for endothelial function. The change ratio of FMD correlated more closely with that of PTX3 than of hsCRP (r =-0.446, P = 0.006 versus r =-0.330, P = 0.050). Significantly more patients with decreased FMD values had increased levels of PTX3 than those of hsCRP at the second measurement compared with the fi rst measurement. Furthermore, the ratio of patients with increased PTX3, but not increased hsCRP, was significantly reduced among those with increased, rather than decreased, FMD values. Endothelial dysfunction might be more accurately predicted by plasma PTX3 levels than by serum hsCRP levels

5-Hydroxymethylcytosine Plays a Critical Role in Glioblastomagenesis by Recruiting the CHTOP-Methylosome Complex

Summary: The development of cancer is driven not only by genetic mutations but also by epigenetic alterations. Here, we show that TET1-mediated production of 5-hydroxymethylcytosine (5hmC) is required for the tumorigenicity of glioblastoma cells. Furthermore, we demonstrate that chromatin target of PRMT1 (CHTOP) binds to 5hmC. We found that CHTOP is associated with an arginine methyltransferase complex, termed the methylosome, and that this promotes the PRMT1-mediated methylation of arginine 3 of histone H4 (H4R3) in genes involved in glioblastomagenesis, including EGFR, AKT3, CDK6, CCND2, and BRAF. Moreover, we found that CHTOP and PRMT1 are essential for the expression of these genes and that CHTOP is required for the tumorigenicity of glioblastoma cells. These results suggest that 5hmC plays a critical role in glioblastomagenesis by recruiting the CHTOP-methylosome complex to selective sites on the chromosome, where it methylates H4R3 and activates the transcription of cancer-related genes. : The development of cancer is driven not only by genetic mutations but also by chromatin and DNA modification changes. Takai et al. now show that proneural glioblastomas contain high levels of 5hmC and TET1. Production of 5hmC is required for the tumorigenicity of glioblastoma cells. Furthermore, 5hmC recruits the CHTOP-methylosome complex to selective sites on the chromosome, where it methylates H4R3 and activates the transcription of cancer-related genes

Elevated Levels of Systemic Pentraxin 3 Are Associated With Thin-Cap Fibroatheroma in Coronary Culprit Lesions : Assessment by Optical Coherence Tomography and Intravascular Ultrasound

Objectives This study sought to determine whether systemic levels of pentraxin 3 (PTX3), a novel inflammatory marker, are associated with thin-cap fibroatheroma (TCFA). Background Biomarkers predicting the presence of TCFA in vivo have not been established. Methods We evaluated 75 patients (stable angina pectoris, n = 47; acute coronary syndrome, n = 28) with de novo culprit lesions who were examined by optical coherence tomography and intravascular ultrasound. We defined TCFA as lipid-rich plaque with a fibrous cap 3.24 ng/ml of PTX3 could predict TCFA with 84% sensitivity and 86% specificity. Conclusions Higher levels of systemic PTX3 are associated with TCFA. Systemic PTX3 levels comprise a useful inflammatory marker that reflects coronary plaque vulnerability