title: [Regulatory role of mechanical stress response in cellular function: development of new drugs and tissue engineering].
abstract: The investigation of mechanotransduction in the cardiovascular system is essentially important for elucidating the cellular and molecular mechanisms involved in not only the maintenance of hemodynamic homeostasis but also etiology of cardiovascular diseases including arteriosclerosis. The present review summarizes the latest research performed by six academic groups, and presented at the 75th Annual Meeting of the Japanese Pharmacological Society. Technology of cellular biomechanics is also required for research and clinical application of a vascular hybrid tissue responding to pulsatile stress. 1) Vascular tissue engineering: Design of pulsatile stress-responsive scaffold and in vivo vascular wall reconstruction (T. Matsuda); 2) Cellular mechanisms of mechanosensitive calcium transients in vascular endothelium (M. Oike et al.); 3) Cross-talk of stimulation with fluid flow and lysophosphatidic acid in vascular endothelial cells (K. Momose et al.); 4) Mechanotransduction of vascular smooth muscles: Rate-dependent stretch-induced protein phosphorylations and contractile activation (K. Obara et al.); 5) Lipid mediators in vascular myogenic tone (I. Laher et al.); and 6) Caldiomyocyte regulates its mechanical output in response to mechanical load (S. Sugiura et al.).
authors.affiliation: Department of Pharmacology, School of Pharmaceutical Sciences, Showa University, Tokyo 142-8555, Japan. krmomose@pharm.showa-u.ac.jp
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Momose
authors.forename: Takehisa
authors.initials: T
authors.lastname: Matsuda
authors.forename: Masahiro
authors.initials: M
authors.lastname: Oike
authors.forename: Kazuo
authors.initials: K
authors.lastname: Obara
authors.forename: Ismail
authors.initials: I
authors.lastname: Laher
authors.forename: Seiryo
authors.initials: S
authors.lastname: Sugiura
authors.forename: Hisayuki
authors.initials: H
authors.lastname: Ohata
authors.forename: Koichi
authors.initials: K
authors.lastname: Nakayama
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000166:cytology*; D015195:Drug Design; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D008246:Lysophospholipids / Q000502:physiology; D040542:Mechanotransduction, Cellular / Q000502:physiology*; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D018994:Myosin Light Chains / Q000378:metabolism; D010766:Phosphorylation; D017346:Protein Serine-Threonine Kinases / Q000502:physiology; D013314:Stress, Mechanical; D023822:Tissue Engineering; D020741:rho GTP-Binding Proteins / Q000378:metabolism; D054460:rho-Associated Kinases
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D008246:Lysophospholipids; D018994:Myosin Light Chains; D017346:Protein Serine-Threonine Kinases; D054460:rho-Associated Kinases; D020741:rho GTP-Binding Proteins; D002118:Calcium