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Developmental regulation of re-uptake of phosphatidylcholine by type II alveolar epithelium
Institution:1. State Key Laboratory of Bioelectronics & National Demonstration Centre for Experimental Biomedical Engineering Education, School of Biological Science and Medical Engineering, Southeast University, Nanjing 210096, PR China;2. College of Materials Science and Technology, Nanjing University of Aeronautics and Astronautics, Nanjing 210016, PR China;3. School of Medicine, Southeast University, Nanjing 210009, PR China;1. Nuclear Medicine and Radiation Biology Research Group, Department of Clinical Medicine, Faculty of Health Science, UiT The Arctic University of Norway, Tromsø, Norway;2. Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Faculty of Medicine and Health Science, Norwegian University of Science and Technology (NTNU), Trondheim, Norway;3. PET Imaging Center Tromsø, University Hospital of North Norway (UNN), Tromsø, Norway;4. Drug Transport and Delivery Research Group, Department of Pharmacy, Faculty of Health Science, UiT The Arctic University of Norway, Tromsø, Norway;5. Department of Biotechnology and Nanomedicine, SINTEF Industry and Department of Circulation and Medical Imaging, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway;1. Department of Pharmaceutics, JSS College of Pharmacy, JSS Academy of Higher Education and Research (JSS AHER), Mysuru 570015, Karnataka, India;2. Department of Pharmaceutical Chemistry, RAK College of Pharmacy, RAK Medical and Health Sciences University, Ras Al Khaimah 11172, United Arab Emirates;3. Department of Pharmaceutics, College of Pharmacy, King Khalid University, Abha 61421, Saudi Arabia;4. Department of Pharmaceutics, RAK College of Pharmacy, RAK Medical and Health Sciences University, Ras Al Khaimah 11172, United Arab Emirates;5. Department of Biochemistry & Molecular Biology, University of Texas Medical Branch, Galveston, TX, United States
Abstract:Type II alveolar epithelia produce, store and secrete pulmonary surfactant, a phospholipid and protein mixture which stabilizes alveoli at low lung volumes and, thereby, prevents alveolar collapse. We determined the developmental changes in the uptake, metabolism and reutilization of surfactant-related phospholipid in primary cultures of type II cells derived from fetal rat lung. Primary cultures of fetal and neonatal type II cells were incubated in media containing labelled liposomes. After the incubation phospholipids were extracted from the cells and uptake of label was analyzed. Re-uptake of radiolabelled dipalmitoyl phosphatidylcholine (DPPC) was concentration-dependent in undifferentiated fetal cells, differentiated fetal cells and neonatal cells. Re-uptake of DPPC by undifferentiated fetal cells was lower than re-uptake by both differentiated fetal and neonatal cells at 15 and 75 μM PC. Binding of DPPC to the cell surface involved a protein interaction, since trypsin was able to dissociate this trypsin-releasable fraction from internalized label. Undifferentiated fetal, differentiated fetal and neonatal cells all exhibited approx. 50% metabolic degradation of internalized phospholipid. Degraded lipids were reutilized in the synthesis of phosphatidylglycerol, but neonatal cells resynthesized twice as much phosphatidylglycerol as did undifferentiated fetal cells. These are the first studies which show that morphologically undifferentiated fetal type II cells are capable of the uptake of surfactant phospholipid as well as the degradation and reutilization of internalized phospholipid. Re-uptake, degradation and reutilization of internalized phospholipid appear to be under developmental control.
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