title: Hydrostatic pressure decreases membrane fluidity and lipid desaturase expression in chondrocyte progenitor cells.
abstract: Membrane biomechanical properties are critical in modulating nutrient and metabolite exchange as well as signal transduction. Biological membranes are predominantly composed of lipids, cholesterol and proteins, and their fluidity is tightly regulated by cholesterol and lipid desaturases. To determine whether such membrane fluidity regulation occurred in mammalian cells under pressure, we investigated the effects of pressure on membrane lipid order of mouse chondrogenic ATDC5 cells and desaturase gene expression. Hydrostatic pressure linearly increased membrane lipid packing and simultaneously repressed lipid desaturase gene expression. We also showed that cholesterol mimicked and cholesterol depletion reversed those effects, suggesting that desaturase gene expression was controlled by the membrane physical state itself. This study demonstrates a new effect of hydrostatic pressure on mammalian cells and may help to identify the molecular mechanisms involved in hydrostatic pressure sensing in chondrocytes.
authors: Division of Regenerative Medical Engineering, Center for Disease Biology and Integrative Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Electronic address: montagne@m.u-tokyo.ac.jp.
authors: Kevin
authors: K
authors: Montagne
authors: Department of Mechanical Engineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan.
authors: Hiroki
authors: H
authors: Uchiyama
authors: Department of Mechanical Engineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan; Department of Bioengineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan.
authors: Katsuko S
authors: KS
authors: Furukawa
authors: Division of Regenerative Medical Engineering, Center for Disease Biology and Integrative Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan; Department of Mechanical Engineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan; Department of Bioengineering, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8656, Japan. Electronic address: ushida@m.u-tokyo.ac.jp.
authors: Takashi
authors: T
authors: Ushida
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D002784:Cholesterol / Q000096:biosynthesis / Q000172:deficiency / Q000378:metabolism; D019902:Chondrocytes / Q000201:enzymology* / Q000473:pathology; D015536:Down-Regulation / Q000235:genetics; D044943:Fatty Acid Desaturases / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics*; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006874:Hydrostatic Pressure; D008560:Membrane Fluidity / Q000502:physiology*; D008563:Membrane Lipids / Q000037:antagonists & inhibitors* / Q000235:genetics; D051379:Mice; D013234:Stem Cells / Q000201:enzymology* / Q000473:pathology; D015854:Up-Regulation / Q000235:genetics
chemical_list: D008563:Membrane Lipids; D002784:Cholesterol; D044943:Fatty Acid Desaturases
keywords: Cholesterol; Desaturase; Hydrostatic pressure; Membrane fluidity