Apoptosis in serum-deprived vascular smooth muscle cells: Evidence for cell volume-independent mechanism
Autor: | Pavel Hamet, Sergei N. Orlov, Dimitri Pchejetski, Alexey V. Pshezhetsky, Sebastien Taurin, Nathalie Thorin-Trescases, Georgy V. Maximov, Andrei B. Rubin |
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Rok vydání: | 2004 |
Předmět: |
Osmosis
Cancer Research Time Factors Vascular smooth muscle medicine.medical_treatment Clinical Biochemistry Pharmaceutical Science Apoptosis Culture Media Serum-Free Muscle Smooth Vascular Ouabain Amino Acid Chloromethyl Ketones Cyclic AMP Mannitol Microscopy Phase-Contrast Enzyme Inhibitors Growth Substances Aorta Caspase 3 Transfection musculoskeletal system Chromatin Cell biology Caspases cardiovascular system Adenovirus E1A Proteins Sodium-Potassium-Exchanging ATPase medicine.drug Biology Adenoviridae Cell Line Dogs medicine Animals Na+/K+-ATPase Cell Size Pharmacology Dose-Response Relationship Drug Growth factor Cell Membrane Colforsin Biochemistry (medical) DNA Cell Biology Rats Kinetics Microscopy Fluorescence Cell culture Potassium |
Zdroj: | Apoptosis. 9:55-66 |
ISSN: | 1360-8185 |
Popis: | Shrinkage is the earliest hallmark of cells undergoing apoptosis. This study examines the role of this phenomenon in the onset of vascular smooth muscle cell (VSMC) apoptosis triggered by growth factor withdrawal. In hyperosmotic media, VSMC showed the same amplitude of shrinkage but were more resistant to apoptosis than endothelial, epithelial and immune system cells. As with growth factor withdrawal, apoptosis in hyperosmotically-shrunken VSMC was sharply potentiated by transfection with E1A-adenoviral protein and was suppressed by activation of cAMP signaling as well as by the pan-caspase inhibitor z-VAD.fmk. Both cell shrinkage and apoptosis in VSMC-E1A treated with hyperosmotic medium were potentiated under sustained Na+, K+ pump inhibition with ouabain that was in contrast to inhibition of apoptosis documented in ouabain-treated, serum-deprived cells. After 1-hr incubation in serum-deprived medium, VSMC-E1A volume declined by approximately 15%. Transfer from hypotonic to control medium decreased VSMC-E1A volume by approximately 25% without any induction of apoptosis. Neither swelling in hyposmotic medium nor dissipation of the transmembrane gradient of K+ and major organic osmolytes protected serum-deprived VSMC-E1A from apoptosis. Thus, our results show that similarly to immune system, endothelial and epithelial cells, extensive VSMC shrinkage in hyperosmotic medium leads to the development of apoptosis. In contrast to hyperosmotic medium, the modest cell volume decrease occurring in serum-deprived VSMC does not contribute to triggering of the apoptotic machinery. |
Databáze: | OpenAIRE |
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