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- Title
Benign Pleural Mesothelial Cells Have Higher Osmotic Water Permeability than Malignant Pleural Mesothelioma Cells and Differentially Respond to Hyperosmolality.
- Authors
Katkova, Liubov E.; Baturina, Galina S.; Bondar, Alexander A.; Jagirdar, Rajesh M.; Hatzoglou, Chrissi; Gourgoulianis, Konstantinos I.; Solenov, Evgeniy I.; Zarogiannis, Sotirios G.
- Abstract
Background/Aims: Cell volume regulation is a critical mechanism for cell homeostasis and depends on the osmotic water permeability (Pf ) of the cell plasma membrane. The Pf of human mesothelial cells is unknown although they contribute to serosal fluid turnover. Methods: In this study we measured the osmotic water permeability of benign human mesothelial cells (MeT-5A) and of epithelioid (M14K) and sarcomatoid (ZL34) malignant pleural mesothelioma (MPM) cells in response to acute hyperosmotic stress. We also assessed the changes in their Pf after preconditioning with 4% glucose for 24 hours. In both cases we also assessed the role of AQP1 inhibition (0.1 mM HgCl2 ) on the Pf . Finally, we assessed corresponding changes in the AQP1 plasma membrane availability by immunofluorescence. Results We report that MeT-5A cells have a significantly higher Pf as compared to M14K and ZL34 MPM cells [4.85E-03±2.37E-03 cm/sec (n=17) versus 2.74E-03±0.74E-03 cm/sec (n=11) and 2.86E-03±0.11E-03 cm/sec (n=11)]. AQP1 inhibition significantly decreased the Pf in all cells lines (p<0.001 in all cases). High glucose preconditioning for 24 hours significantly increased MeT-5A Pf (p<0.001), did not influence M14K Pf (p=0.19) and significantly reduced ZL34 Pf (p=0.02). Comparing cell lines after high glucose preconditioning, MeT-5A Pf was significantly higher than that of M14K and ZL34 MPM cells and the AQP1 inhibition effect was significant in MeT-5A and M14K cells. These results were corroborated by AQP1 immunofluorescence. Conclusion: We provide evidence for a differential regulation of Pf in benign and MPM cells that require further mechanistic investigation.
- Publication
Cellular Physiology & Biochemistry (Cell Physiol Biochem Press GmbH & Co. KG), 2019, Vol 52, Issue 4, p869
- ISSN
1015-8987
- Publication type
Article
- DOI
10.33594/000000060