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Anti‐endothelial cell antibodies (AECA) in pulmonary arterial hypertension (PAH)
Author(s) -
Morrow Rebekah,
Fagan Karen A.,
Cioffi Donna L.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.873.4
Subject(s) - endothelial stem cell , connective tissue disease , blot , endothelial dysfunction , autoimmune disease , antibody , medicine , endothelium , immunology , vascular disease , pathology , reactive oxygen species , immune system , pulmonary hypertension , chemistry , biology , in vitro , microbiology and biotechnology , biochemistry , gene
PAH is a fatal disease that results in right heart failure. PAH pathology is unclear, but endothelial activation and immune responses contribute to vascular remodeling. AECA are found in many autoimmune disorders and both idiopathic and connective tissue disease‐associated PAH. In autoimmune vasculitides, AECA activate endothelial cells through increased reactive oxygen species (ROS) production. While the effects of AECA on endothelial cells have been studied in some diseases, the effects of AECA from PAH on pulmonary endothelial cells are unknown. We sought to determine whether AECA bind and increase ROS in pulmonary endothelial cells. Methods Western blots were performed using membrane fractions of human pulmonary and systemic endothelial cells. Blots were treated with serum from PAH patients or healthy controls. Fluorescence microscopy was used to assess the effects of AECA on ROS production in cells treated with IgG from PAH patients or healthy controls. Results While some bands were found in both PAH and healthy subjects, a band of 37 kD was seen in pulmonary microvascular endothelial cells when blots were treated with PAH serum. Cells treated with IgG from healthy controls showed no increase in ROS but PAH IgG elicited an increase. These data suggest that some AECA from PAH bind to pulmonary endothelial cells and may lead to ROS generation. Supported by 5R00HL089361 and 5T32HL076125‐8.