We studied the changes in thiol status in mouse retina lacking aA-or aB crystallin

and interferon-gamma-inducible 10 kD protein were present as detected by ELISA. All three factors were also detected at the tissue level by immunohistochemistry. In addition, the receptor for PF4 and IP-10, CXCR3, was found in the PEA surgical material with high expression levels, particularly in the distal areas, as compared with healthy lung tissue. CXCR3 expression at the mRNA level was likewise higher in CTEPH tissue from the distal parts of PEA as compared with healthy lungs. 4 Angiostatic Factors in CTEPH IP-10 treatment increased Luteolin 7-O-β-D-glucoside Calcium influx after 24 h significantly compared to control. Angiostatic factors lead to endothelial dysfunction The effects of IP-10, PF4 and collagen type I on hPAECs were further investigated by means of migration assay. PF4 treatment resulted in a significantly reduced migration, similar to collagen type I treatment. Interestingly, treatment with IP-10 did not induce alteration in wound closure compared to untreated cells. Similarly, PF4 and collagen type I treatment induced a significant decrease in proliferation compared to untreated cells. In contrast, IP10 increased the hPAEC proliferation. Loop formation, tested with an in vitro angiogenesis assay, was significantly decreased by all treatments as compared to control. The strongest effect was observed in the collagen type I-treated hPAECs. Discussion Chronic thromboembolic pulmonary hypertension is a rare and late complication of venous thromboembolism. A fresh pulmonary embolus normally gets dissolved by fibrinolysis, macrophages and by recanalization. In CTEPH patients, the recanalization does not occur or is incomplete resulting in elevation of pulmonary vascular resistance and secondary remodeling of non-occluded vessels. In our study, we investigated endothelial cells from surgical PEA material, compared them with control hPAECs and tested the effect of mediators secreted by the PEA material on hPAECs. Our readouts included calcium homeostasis, proliferation, migration and vessel formation. Similar to previous studies, we observed newly formed vessels in the surgical PEA material. This neovascularization/ recanalization has been suggested to be due to endothelial progenitor cells and/or hPAECs and pulmonary artery smooth muscle cells migrating from the pulmonary artery or from the systemic circulation and being trapped in the thrombotic clot. Calcium is a key regulatory molecule for endothelial function. We observed a significant rise in the basal calcium level of the CTEPH-hECs as compared to the hPAECs. Furthermore, in our study histamine challenge led to a stronger response in the CTEPH-hECs as compared to hPAECs. We applied a calcium ATPase inhibitor to induce depletion of the calcium stores and to identify the reason for this calcium rise. By measuring the readmission of the external calcium, the store-operated calcium influx was quantified and compared to healthy control cells. With this tool, possible dysfunctions either in calcium channels of the plasma membrane or in the calcium stores can be detected. The increased calcium depletion of the CTEPH-hECs compared to hPAECs showed that these cells accumulate more calcium in their stores, which is a sign of altered calcium homeostasis. The readmission of external calcium was greater in the CTEPH-hECs Angiostatic Factors in CTEPH 6 Angiostatic Factors in CTEPH compared to control cells. One possible reason for this increase could be the higher expression or sensitivity of transient recep