3 results match your criteria: "Free University Berlin and the Humboldt University Berlin[Affiliation]"
Mannose-6-phosphate attenuates acute lung injury by competitive release of acid sphingomyelinase from the mannose-6-phosphate receptor in endothelial caveolae.
Eur Respir J
February 2025
Institute of Physiology, Charité - Universitätsmedizin Berlin, Free University Berlin and the Humboldt University Berlin, Berlin, Germany.
Background: Platelet-activating factor (PAF)-induced pulmonary endothelial barrier failure is mediated by acid sphingomyelinase (ASM) translocation to caveolae. ASM, however, lacks a transmembrane domain for anchoring inside caveolae. We hypothesized that ASM may anchor to cation-independent mannose-6-phosphate receptor (CI-M6PR) in caveolae from where it can be competitively released by M6P.
View Article and Find Full Text PDFRUNX2 is stabilised by TAZ and drives pulmonary artery calcification and lung vascular remodelling in pulmonary hypertension due to left heart disease.
Eur Respir J
November 2024
Institute for Physiology, Charité - Universitätsmedizin Berlin, corporate member of the Free University Berlin and the Humboldt University Berlin, Berlin, Germany.
Article Synopsis
- Calcification in pulmonary hypertension associated with left heart disease appears to be influenced by the interaction between RUNX2 and TAZ, which are key regulators in osteogenic processes.
- Significant vascular calcification was observed in both patients and rat models, with elevated levels of RUNX2 and TAZ.
- Inhibiting TAZ or RUNX2 effectively reduced vascular calcification and the progression of pulmonary hypertension in the rat model, suggesting potential therapeutic targets.
Stimulation of the EP receptor causes lung oedema by activation of TRPC6 in pulmonary endothelial cells.
Eur Respir J
October 2022
Institute for Physiology, Charité - Universitätsmedizin Berlin, Corporate Member of the Free University Berlin and the Humboldt University Berlin, Berlin, Germany
Background: Prostaglandin E (PGE) increases pulmonary vascular permeability by activation of the PGE receptor 3 (EP), which may explain adverse pulmonary effects of the EP/EP receptor agonist sulprostone in patients. In addition, PGE contributes to pulmonary oedema in response to platelet-activating factor (PAF). PAF increases endothelial permeability by recruiting the cation channel transient receptor potential canonical 6 (TRPC6) to endothelial caveolae acid sphingomyelinase (ASMase).
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