PL-II Lipid Mediators and Protein Kinase C Activation for Intracellular Signalling

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概要

• 論文の詳細を見る

• Inositol phospholipid (PI) hydrolysis, initiated by either receptor stimulation or Ca^<2+> -gate opening, was once thought to be the sole mechanism to produce diacylglycerol that links extracellular signals to intracellular events through activation of protein kinase C(PKC). It is becoming clear that, upon stimulation of cell surface receptors, some other membrane phospholipids may also be degraded to produce additional lipid mediators. For instance, many signals induce hydrolysis of choline phospholipid (PC) by activating phospholipase A_2, and generate two additional chemicals, free cis-unsaturated fatty acid and lysophosphatidylcholine (lysoPC), both of which are effective to enhance subsequent cellular responses. Several cis-unsaturated fatty acids including oleic, linoleic, and linolenic acids, when added exogenously, greatly enhance diacylglycerol-dependent activation of PKC both in cell-free enzymatic systems and in intact cells such as platelets. The cellular responses are potentiated concomitantly. A membrane-permeant diacylglycerol is essential for this action of fatty acids. Kinetic analysis in vitro and with the Ca^<2+> -sensitive fluorescent dye fura 2 indicates that cis-unsaturated fatty acids markedly increase an apparent affinity of PKC activation to Ca^<2+>, and causes nearly full activation of the enzyme without a large increase in the intracellular Ca^<2+> concentration. LysoPC, the other half of the PC molecule resulting from phospholipase A_2 activation, also potentiates cellular responses, particularly those in long-term such as cell proliferation and differentiation. Namely, lysoPC dramatically enhances the activation, of human resting T-lymphocytes and differentiation of HL-60 cells to macrophages. LysoPC is active only when diacylglycerol or phorbol ester is present, suggesting that this lysophospholipid interacts with PKC pathway. Plausible evidence available to date suggests that the signal-induced

• 日本組織細胞化学会の論文
• 1993-10-28

著者

• TANAKA C.

  Department of Dental Materials, School of Dentistry, University of Sao Paulo

• SAITO N.

  Department of Obstetrics and Gynecology, Saiseikai Fukuoka Central Hospital

• Asaoka Y.

  Biosignal Research Center Kobe University

• Nishizuka Y.

  Departments Of Biochemistry School Of Medicine Kobe University:biosignal Research Center Kobe Univer

• Nakamura S.

  Departments of Biochemistry, School of Medicine, Kobe University

• Ogita K.

  Departments of Biochemistry, School of Medicine, Kobe University

• Kikkawa U.

  Biosignal Research Center, Kobe University

• Kikkawa U.

  Biosignal Research Center Kobe University

• Ogita K.

  Departments Of Biochemistry School Of Medicine Kobe University

• Ogita K.

  Department Of Pediatric Surgery Reproductive And Developmental Medicine Graduate School Of Medical S

• Saito N.

  Department of Chemistry, University of Oregon

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