image: A human pulmonary artery (<300 micrometers in diameter) from the lung of a patient with idiopathic pulmonary arterial hypertension, shows increased levels of Nogo-B (red) throughout the vascular wall, including the smooth muscle cells (green). The nuclei are stained blue with DAPI and colocalization of Nogo-B in smooth muscle cells is shown in yellow. Nogo-B is not present in pulmonary arteries from patients without pulmonary hypertension. Induction of Nogo-B disrupts the endoplasmic reticulum-mitochondria unit in smooth muscle cells, resulting in decreased intramitochondrial calcium, inhibition of calcium-sensitive mitochondrial enzymes and suppression of mitochondrial-dependent cell death (apoptosis), facilitating the over-proliferation of cells within the pulmonary arterial wall, which characterizes this deadly disease. This image relates to a paper that appeared in the June 22, 2011, issue of Science Translational Medicine, published by AAAS. The paper, by Dr. G. Sutendra of the University of Alberta in Edmonton, AB, Canada and colleagues, was titled, "The Role of Nogo and the Mitochondria–Endoplasmic Reticulum Unit in Pulmonary Hypertension." view more
Credit: Image © Science/AAAS