TY - JOUR T1 - Late-breaking abstract: Intracellular mechanisms behind the effect of C-reactive protein on proximal vascular cells of CTEPH patients JF - European Respiratory Journal JO - Eur Respir J VL - 38 IS - Suppl 55 SP - 3430 AU - Marijke Wynants AU - Rozenn Quarck AU - Bart Meyns AU - Marion Delcroix Y1 - 2011/09/01 UR - http://erj.ersjournals.com/content/38/Suppl_55/3430.abstract N2 - Chronic thromboembolic pulmonary hypertension (CTEPH) is associated with vascular remodeling and inflammation. Our latest results showed that C-reactive protein (CRP) could contribute to vascular remodeling and endothelial dysfunction in pulmonary vascular cells of CTEPH patients.We aimed to investigate the intracellular mechanism responsible for the effect of CRP on CTEPH pulmonary vascular cells.Pulmonary proximal arterial endothelial (EC) and smooth muscle cells (SMC) were isolated from patients with CTEPH. After stimulation with CRP, total RNA was extracted from CTEPH-EC and CTEPH-SMC and first stand cDNA was generated. A RT2 profiler PCR Array (SABioscience) was used to evaluate the expression of 84 key genes related to NFκB-mediated signal transduction.Different genes from the NFκB pathway were up- or downregulated in CRP-stimulated CTEPH-EC and CTEPH-SMC. In CRP-stimulated EC isolated from 5 different CTEPH patients, the serotonin receptor 1B was significantly downregulated (p=0.0089) compared to not stimulated CTEPH-EC. CRP significantly downregulated the toll-like receptor 4 (p=0.032) and inhibitor of kappa B light polypepetide (p=0.025) in CTEPH-EC. In CRP-stimulated SMC isolated from 4 different CTEPH patients, mucosa associated lymphoid tissue 1 (p=0.038) and B-cell lymphoma 10 (p=0.012) were significantly upregulated.These results suggest an involvement of the NFκB pathway in mediating the effects of CRP on vascular cells of CTEPH patients. ER -