TASK-1 potassium channel is not critically involved in mediating hypoxic pulmonary vasoconstriction of murine intra-pulmonary arteries.

The two-pore domain potassium channel KCNK3 (TASK-1) is expressed in rat and human pulmonary artery smooth muscle cells. There, it is associated with hypoxia-induced signalling, and its dysfunction is linked to pathogenesis of human pulmonary hypertension. We here aimed to determine its role in hypoxic pulmonary vasoconstriction (HPV) in the mouse, and hence the suitability of this model for further mechanistic investigations, using appropriate inhibitors and TASK-1 knockout (KO) mice.

COPD-associated pulmonary hypertension: clinical implications and current methods for treatment.

Chronic obstructive pulmonary disease is the fourth leading cause of death worldwide, one serious complication being pulmonary hypertension, which occurs in up to 30% of patients and increases mortality drastically. Difficulties in diagnosis and the unclear beneficial effects of PH-specific therapy have hitherto resulted in the absence of approved therapies. Consequently, PH and right heart failure in COPD are still currently treated according to symptoms and not underlying cause Areas covered: This review focuses on the current knowledge of its pathogenesis, clinical picture, diagnosis as well as methods for treatment Expert commentary: Since PH-COPD is an orphan disease with grievous consequences, and diagnosis as well as the right choice of possible treatment is crucial, referral to an expert center in cases of suspicion is necessary.

Anti-human neutrophil antigen-3a induced transfusion-related acute lung injury in mice by direct disturbance of lung endothelial cells.

Objective: Antibodies against human neutrophil antigen-3a (HNA-3a) located on choline transporter-like protein 2 induce severe transfusion-related acute lung injury (TRALI). This study aims to identify the mechanism implicated in anti-HNA-3a-mediated TRALI.

Approach And Results: Our analysis shows that anti-HNA-3a recognizes 2 choline transporter-like protein 2 isoforms (P1 and P2) on human microvascular endothelial cells from lung blood vessels but reacts only with the P1 isoform on neutrophils.