Serum Caveolin-1 as a Novel Biomarker in Idiopathic Pulmonary Artery Hypertension.

Pulmonary arterial hypertension (PAH) is a rare disease but with significant morbidity and high mortality. There is no specific way to diagnose PAH. Thus, an easy used with good sensitivity and specificity biomarker of PAH is highly desirable to aid in the screening, diagnosis, and follow-up. Caveolin-1 (Cav1) is the structural protein of caveolae and is highly expressed in type I pneumocytes. Lungs tissues from idiopathic PAH (IPAH) patients showed decreased expression of Cav1 in vascular endothelial cells. Therefore, we developed a direct sandwich immunoassay for the determination of Cav1 in IAPH patient's serum. The result disclosed serum Cav1 level was significantly lower in IPAH than control groups. Using serum Cav1, 17.17 pg/mL as a cutoff value, the sensitivity was 0.59 and the specificity was 1.0. There were two major findings in our results. First, serum Cav1 might be a novel biomarker in the diagnosis of IPAH with fare sensitivity and good specificity. Second, Cav1 might be used to make differential diagnosis between COPD-PH and IPAH group.

Caffeic acid phenethyl ester inhibits proliferation and migration, and induces apoptosis in platelet-derived growth factor-BB-stimulated human coronary smooth muscle cells.

BACKGROUND/AIMS: Restenosis after a percutaneous coronary intervention (PCI) during treatment for coronary artery disease is closely related to smooth muscle cell (SMC) proliferation and migration. In this study, we investigated the effects of caffeic acid phenethyl ester (CAPE) and its underlying mechanism on human coronary SMCs (HCSMCs) after platelet-derived growth factor-BB (PDGF-BB) stimulation in vitro. METHODS AND RESULTS: The results showed that CAPE inhibited proliferation and migration, and induced apoptosis. Concomitantly, CAPE inhibited activation of AKT1, MEK1 and ERK1/2 signaling molecules at 10-60 min after CAPE treatment. As revealed by flow cytometry, DNA fragmentation and TUNEL assay, the cells accumulated at the sub-G(1) phase, and cell apoptosis was observed after 30 and 90 µM CAPE treatment for 72 h. CAPE triggered the release of cytochrome c from mitochondria to cytosol, upregulated the proapoptotic gene Bax and downregulated the antiapoptotic gene Bcl-2. Upregulation of caspase-9 and caspase-3 indicated that CAPE precipitated the mitochondrion-dependent apoptotic signaling pathway. CONCLUSIONS: These results provide a molecular explanation for the antiproliferation, antimigration and proapoptotic effects of CAPE on HCSMCs after PDGF-BB stimulation.

Immediate change in pulmonary venous flow pattern after deployment of occluder device for atrial septal defect.

Transcatheter closure of a secundum defect using a septal occluder is a safe and effective procedure based on long-term follow-up, but no clinical studies have examined immediate hemodynamic changes. We evaluated pulmonary venous flow velocity pattern before and immediately after deployment of the Amplatzer septal occluder for closure of atrial septal defect. From May 2003 to January 2005, 48 patients with secundum atrial septal defect received transcatheter closure with complete occlusion. Patients were divided into two groups according to age: pediatric group, under 16 years (n = 30, age 7.3 +/- 3.2 years), and adult group, 16 years or older (n = 18, age 30.1 +/- 11.4 years). Pulmonary venous flow pattern was recorded by transesophageal echocardiography before and immediately after occluder deployment. Immediately after deployment in both patient groups, pulmonary vein systolic (S) and diastolic (D) wave velocity decreased, but atrial reversal (AR) wave velocity increased. In the pediatric group, S-wave was 56.1 +/- 17.1 versus 35.5 +/- 11.3 cm/sec (P < 0.001); D-wave was 57.6 +/- 12.5 versus 42.9 +/- 11.8 cm/sec (P < 0.001); and AR wave velocity was 12.2 +/- 3.8 versus 15.5 +/- 4.1 cm/sec (P < 0.001). In the adult group, S-wave was 48.4 +/- 13.7 versus 32.7 +/- 10.3 cm/sec (P < 0.001); D-wave was 51.9 +/- 11.7 versus 38.0 +/- 8.5 m/sec (P < 0.001); and AR wave velocity was 12.1 +/- 4.1 versus 16.2 +/- 4.9 cm/sec (P < 0.001). Comparison of pulmonary venous flow before and immediately after deployment of the Amplatzer septal occluder provides an excellent model to evaluate the influence of an atrial communication on pulmonary venous flow. Pulmonary venous forward flow decreases following atrial septal defect (ASD) closure.