Anti-TBXA2R monoclonal antibody, clone FQS8447

Prostaglandins (PGD(2), PGE(2), PGF(2 alpha), and PGI(2)) and thromboxane A(2) (TXA(2)) are biologically active molecules derived from the metabolism of arachidonic acid by cyclooxygenases. They produce a wide variety of physiological and pathophysiological effects mediated through specific G protein-coupled cell surface receptors. In this study, we have mapped the chromosomal positions of the human genes that encode the PGE(2) receptor subtypes (PTGER1, PTGER2, and PTGER3), the PGF(2 alpha) receptor (PTGFR), the PGI(2) receptor (PTGIR), and the TXA(2) receptor (TBXA2R) using in situ hybridization. The PTGER1, TBXA2R, and PTGIR genes mapped to chromosome 19 at positions 19p13.1, 19p13.3, and 19q13.3, respectively. The PTGFR and PTGER3 genes mapped to chromosome 1 at positions 1p31.1 and 1p31.2, respectively, and PTGER2 gene mapped to chromosome band 5p13.1. (C) 1995 Academic Press, Inc.

Group III pulmonary hypertension is observed in patients with chronic lung diseases such as chronic obstructive pulmonary disease or idiopathic pulmonary fibrosis. Pulmonary hypertension (PH) develops as a result of extensive pulmonary vascular remodelling and resultant changes in vascular tone that can lead to right ventricle hypertrophy. This eventually leads to right heart failure, which is the leading indicator of mortality in patients with idiopathic pulmonary fibrosis. Treatments for groupIII PH are not available, in part owing to a lack of viable animal models. Here, we have evaluated the cardiovascular changes in a model of lung fibrosis and PH. Data obtained from this study indicated that structural alterations in the right heart, such as right ventricular wall hypertrophy, occurred as early as day14, and similar increases in right ventricle chamber size were seen between days21 and 28. These structural changes were correlated with decreases in the systolic function of the right ventricle and right ventricular cardiac output, which also occurred between the same time points. Characterization of pulmonary artery dynamics also highlighted that PH might be occurring as early as day21, indicated by reductions in the velocity-time integral; however, evidence for PH is apparent as early as day 7, indicated by the significant reduction in pulmonary acceleration time values. These changes are consistent with evidence of vascular remodelling observed histologically starting on day 7. In addition, we report hyperactivity of bleomycin-exposed pulmonary arteries to a thromboxaneA2 receptor (Tbxa2r) agonist.