tailieunhanh - Báo cáo y học: " GDF-15 is abundantly expressed in plexiform lesions in patients with pulmonary arterial hypertension and affects proliferation and apoptosis of pulmonary endothelial cells"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:" GDF-15 is abundantly expressed in plexiform lesions in patients with pulmonary arterial hypertension and affects proliferation and apoptosis of pulmonary endothelial cells. | Nickel et al. Respiratory Research 2011 12 62 http content 12 1 62 RESPIRATORY RESEARCH RESEARCH Open Access GDF-15 is abundantly expressed in plexiform lesions in patients with pulmonary arterial hypertension and affects proliferation and apoptosis of pulmonary endothelial cells 1Ỷ 2Ỷ 3 2 2 2 Nils Nickel Danny Jonigk Tibor Kempf Clemens L Bockmeyer Lavinia Maegel Johanna Rische 2 2 111 1 Florian Laenger Ulrich Lehmann Clemens Sauer Mark Greer Tobias Welte Marius M Hoeper and Heiko A Golpon1 Abstract Background Growth-differentiation factor-15 GDF-15 is a stress-responsive transforming growth factor-p-related cytokine which has recently been reported to be elevated in serum of patients with idiopathic pulmonary arterial hypertension IPAH . The aim of the study was to examine the expression and biological roles of GDF-15 in the lung of patients with pulmonary arterial hypertension PAH . Methods GDF-15 expression in normal lungs and lung specimens of PAH patients were studied by real-time RT-PCR and immunohistochemistry. Using laser-assisted micro-dissection GDF-15 expression was further analyzed within vascular compartments of PAH lungs. To elucidate the role of GDF-15 on endothelial cells human pulmonary microvascular endothelial cells HPMEC were exposed to hypoxia and laminar shear stress. The effects of GDF-15 on the proliferation and cell death of HPMEC were studied using recombinant GDF-15 protein. Results GDF-15 expression was found to be increased in lung specimens from PAH patients com-pared to normal lungs. GDF-15 was abundantly expressed in pulmonary vascular endothelial cells with a strong signal in the core of plexiform lesions. HPMEC responded with marked upregulation of GDF-15 to hypoxia and laminar shear stress. Apoptotic cell death of HPMEC was diminished whereas HPMEC proliferation was either increased or decreased depending of the concentration of recombinant GDF-15 protein. Conclusions GDF-15 expression is increased in PAH