Differential alterations of ethanolamine and choline phosphoglyceride metabolism by clofibrate and retinoic acid in human fibroblasts are not mediated by phorbol ester-sensitive protein kinase C.

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  • Author(s): Mandla SG;Mandla SG; Byers DM; Ridgway ND; Cook HW
  • Source:
    Lipids [Lipids] 1996 Jul; Vol. 31 (7), pp. 747-55.
  • Publication Type:
    Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Wiley Subscription Services, Inc Country of Publication: United States NLM ID: 0060450 Publication Model: Print Cited Medium: Print ISSN: 0024-4201 (Print) Linking ISSN: 00244201 NLM ISO Abbreviation: Lipids Subsets: MEDLINE
    • Publication Information:
      Publication: 2018- : Hoboken, NJ : Wiley Subscription Services, Inc.
      Original Publication: Chicago, American Oil Chemists' Society.
    • Subject Terms:
      Sulfonamides*; Clofibrate/*pharmacology ; Ethanolamines/*metabolism ; Hypolipidemic Agents/*pharmacology ; Phosphatidylcholines/*metabolism ; Protein Kinase C/*metabolism ; Tretinoin/*pharmacology; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/pharmacology ; Carcinogens/pharmacology ; Enzyme Inhibitors/pharmacology ; Ethanolamine ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Isoquinolines/pharmacology ; Phospholipids/metabolism ; Protein Kinase C/antagonists & inhibitors ; Protein Kinase C/drug effects ; Skin/cytology ; Staurosporine/pharmacology ; Tetradecanoylphorbol Acetate/pharmacology ; Time Factors
    • Abstract:
      Peroxisomal proliferators and retinoids have been reported to interact to regulate lipid metabolism, particularly beta-oxidation of fatty acids. Based on postulated interactions of these agents at the levels of receptors and response elements, we examined whether interactions exist between the peroxisomal proliferator, clofibrate (CLF), and retinoic acid (RA) in modulation of phospholipid turnover in cultured human skin fibroblasts. Treatment of cultured cells with either 25 microM CLF or 1 microM RA alone decreased [14C]ethanolamine incorporation into ethanolamine phosphoglycerides (EPG) by 20-30%, and simultaneous exposure to both agents resulted in additive inhibition. By contrast, [3H]choline incorporation into phospholipid was stimulated 5-30% by incubation with either agent; when CLF and RA were administered together, the stimulatory effects were additive. Different types of pulse-chase studies examining effects on uptake, biosynthesis, and degradation of labelled phospholipids indicated stimulation of EPG degradation and inhibition of phosphatidylcholine degradation by CLF; no effect on catabolism of either phospholipid was observed with RA. Combinations of modifiers of protein kinase activity [4 beta-12-O-tetradecanoylphorbol-13-acetate (beta-TPA), 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride, N-(2'-guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride, bis-indolylmaleimide, staurosporine indicated that beta-TPA-responsive protein kinases were not involved. Accordingly, CLF and RA regulate biosynthesis and degradation of ethanolamine and choline phosphoglycerides in cultured skin fibroblasts by different mechanisms that do not involve classical protein kinase C (PKC) isoforms, even though turnover of phospholipids generating lipid activators of PKC occurs.
    • References:
      FASEB J. 1991 Dec;5(15):3092-9. (PMID: 1743440)
      J Biol Chem. 1994 Jun 3;269(22):15399-402. (PMID: 7910825)
      Biochim Biophys Acta. 1994 Jul 21;1222(3):492-500. (PMID: 8038220)
      Biochim Biophys Acta. 1992 Apr 30;1135(1):84-90. (PMID: 1591274)
      J Biol Chem. 1995 Mar 17;270(11):5901-8. (PMID: 7890721)
      Mol Pharmacol. 1992 Feb;41(2):387-92. (PMID: 1538715)
      Crit Rev Clin Lab Sci. 1992;29(3-4):185-215. (PMID: 1336957)
      Annu Rev Pharmacol Toxicol. 1989;29:145-63. (PMID: 2658768)
      Neurochem Res. 1989 Mar;14(3):279-84. (PMID: 2542824)
      FEBS Lett. 1993 Jan 2;315(1):33-7. (PMID: 8416807)
      Biochem Biophys Res Commun. 1992 Sep 16;187(2):657-63. (PMID: 1530623)
      Biochemistry. 1984 Oct 9;23 (21):5036-41. (PMID: 6238627)
      J Neurochem. 1993 Apr;60(4):1414-21. (PMID: 8455032)
      Biochem J. 1990 Jun 15;268(3):719-24. (PMID: 2363706)
      Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1440-4. (PMID: 8381967)
      Biochim Biophys Acta. 1984 Jun 25;779(2):217-51. (PMID: 6329299)
      Biochimie. 1993;75(3-4):251-6. (PMID: 8389594)
      J Biol Chem. 1995 Feb 24;270(8):3836-40. (PMID: 7876127)
      Biochim Biophys Acta. 1994 Sep 15;1214(2):161-70. (PMID: 7918596)
      J Biol Chem. 1994 Jul 22;269(29):18767-72. (PMID: 7913466)
      Drug Metab Dispos. 1992 Nov-Dec;20(6):779-91. (PMID: 1362927)
      Carcinogenesis. 1994 Apr;15(4):701-5. (PMID: 8149483)
      J Biol Chem. 1993 Aug 25;268(24):17830-6. (PMID: 8394351)
      J Biol Chem. 1991 Aug 25;266(24):15771-81. (PMID: 1874734)
      J Biol Chem. 1994 Mar 25;269(12):8675-9. (PMID: 8132595)
      Biochim Biophys Acta. 1994 Jan 3;1210(2):187-94. (PMID: 8280769)
      Crit Rev Toxicol. 1983;12(1):1-58. (PMID: 6360536)
      Neurosci Lett. 1992 May 25;139(2):183-7. (PMID: 1608547)
      Biochem Biophys Res Commun. 1995 Jan 5;206(1):429-36. (PMID: 7818548)
      Ann N Y Acad Sci. 1993 Jun 11;684:157-73. (PMID: 8391237)
      J Biol Chem. 1989 Feb 15;264(5):2746-52. (PMID: 2914928)
      Biol Cell. 1993;77(1):67-76. (PMID: 8390886)
      Neurochem Res. 1994 Apr;19(4):457-62. (PMID: 8065502)
      J Biol Chem. 1985 Aug 25;260(18):10039-43. (PMID: 3160705)
      Proc Natl Acad Sci U S A. 1994 Jun 7;91(12):5252-6. (PMID: 8202477)
      Biochim Biophys Acta. 1992 Jan 24;1123(2):170-6. (PMID: 1739748)
      Trends Biochem Sci. 1994 Feb;19(2):73-7. (PMID: 8160269)
      Int J Biochem. 1990;22(12):1413-8. (PMID: 2276415)
      J Cell Biochem. 1995 Feb;57(2):362-70. (PMID: 7759571)
      Biochim Biophys Acta. 1994 Jun 2;1212(3):311-8. (PMID: 8199202)
      Nature. 1995 Mar 9;374(6518):118-9. (PMID: 7533261)
      Eur J Biochem. 1992 Oct 1;209(1):467-73. (PMID: 1327780)
      J Biol Chem. 1951 Nov;193(1):265-75. (PMID: 14907713)
      Science. 1992 Oct 23;258(5082):607-14. (PMID: 1411571)
      FEBS Lett. 1989 Jul 3;250(2):205-10. (PMID: 2753129)
      Biochim Biophys Acta. 1992 Jun 22;1126(2):125-34. (PMID: 1627614)
      Biochem Biophys Res Commun. 1994 Oct 14;204(1):112-9. (PMID: 7945349)
      Proc Natl Acad Sci U S A. 1976 Jun;73(6):2043-6. (PMID: 180535)
      Biochim Biophys Acta. 1994 May 13;1212(2):137-51. (PMID: 8180240)
      Nature. 1992 Aug 27;358(6389):771-4. (PMID: 1324435)
      Biochem J. 1991 Dec 1;280 ( Pt 2):387-91. (PMID: 1747111)
    • Accession Number:
      0 (Carcinogens)
      0 (Enzyme Inhibitors)
      0 (Ethanolamines)
      0 (Hypolipidemic Agents)
      0 (Isoquinolines)
      0 (Phosphatidylcholines)
      0 (Phospholipids)
      0 (Sulfonamides)
      5688UTC01R (Tretinoin)
      5KV86114PT (Ethanolamine)
      84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine)
      91742-10-8 (N-(2-guanidinoethyl)-5-isoquinolinesulfonamide)
      EC 2.7.11.13 (Protein Kinase C)
      H88EPA0A3N (Staurosporine)
      HPN91K7FU3 (Clofibrate)
      NI40JAQ945 (Tetradecanoylphorbol Acetate)
    • Publication Date:
      Date Created: 19960701 Date Completed: 19961217 Latest Revision: 20190814
    • Publication Date:
      20221213
    • Accession Number:
      10.1007/BF02522891
    • Accession Number:
      8827698