The increase of choline acetyltransferase activity by docosahexaenoic acid in NG108-15 cells grown in serum-free medium is independent of its effect on cell growth
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
- MeSH
- buněčné dělení účinky léků MeSH
- buněčné linie MeSH
- cholin-O-acetyltransferasa metabolismus MeSH
- kultivační média bez séra MeSH
- kyseliny dokosahexaenové farmakologie MeSH
- lidé MeSH
- oxidační stres MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- cholin-O-acetyltransferasa MeSH
- kultivační média bez séra MeSH
- kyseliny dokosahexaenové MeSH
We investigated the influence of the polyunsaturated docosahexaenoic acid (22:6n-3; DHA) on the constitutive expression of choline acetyltransferase (ChAT) in native and induced expression in differentiated cholinergic cells NG108-15 grown in serum-free medium. Elimination of serum-derived trophic support resulted in growth arrest and a strong decrease of ChAT activity. In either conditions, DHA largely rescued general indicators of cell growth and function, and partially prevented the decrease of ChAT activity. However, the maximal effect on general cell state in native and differentiated cells, and ChAT activity in native cells, was reached at or below 10 mumol/l of DHA. In contrast, maximal induction of ChAT activity in differentiated cells required about six times higher concentrations of DHA. These data thus demonstrate stimulatory effect of DHA on ChAT activity that is independent of its general cell protective properties.
Zobrazit více v PubMed
J Nutr. 2005 May;135(5):1008-13 PubMed
Metab Brain Dis. 2000 Mar;15(1):45-64 PubMed
Methods Enzymol. 1985;109:316-41 PubMed
Nat Cell Biol. 2005 Nov;7(11):1118-23 PubMed
Neuron. 2004 Sep 2;43(5):596-9 PubMed
J Lipid Res. 2003 Dec;44(12):2221-33 PubMed
J Neurochem. 1995 Aug;65(2):939-42 PubMed
Brain Res. 2005 Nov 16;1062(1-2):101-10 PubMed
Trends Neurosci. 2002 Feb;25(2):79-84 PubMed
Nat Neurosci. 2003 Apr;6(4):345-51 PubMed
Science. 1982 Jul 30;217(4558):408-14 PubMed
Pharmacol Biochem Behav. 1997 Dec;58(4):1123-9 PubMed
Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1941-6 PubMed
J Neurosci. 1997 Oct 1;17(19):7288-96 PubMed
Neurochem Res. 2001 Sep;26(8-9):1079-84 PubMed
Brain Res. 2001 Aug 10;910(1-2):134-41 PubMed
J Mol Neurosci. 2001 Apr-Jun;16(2-3):223-7; discussion 279-84 PubMed
J Biol Chem. 2002 Mar 15;277(11):8755-8 PubMed
J Neurol Neurosurg Psychiatry. 1999 Feb;66(2):137-47 PubMed
Gen Pharmacol. 1997 Sep;29(3):401-7 PubMed
J Hum Nutr Diet. 2004 Oct;17 (5):449-59 PubMed
Anal Biochem. 1977 Dec;83(2):346-56 PubMed
Proc Natl Acad Sci U S A. 1999 Sep 14;96(19):10893-8 PubMed
J Neurosci. 2000 Apr 1;20(7):2589-601 PubMed
Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6826-31 PubMed
Neurobiol Aging. 2003 Mar-Apr;24(2):233-43 PubMed
J Lipid Res. 2003 Aug;44(8):1545-51 PubMed
Neuroscience. 2003;119(4):999-1012 PubMed
Brain Res Bull. 2001 Mar 1;54(4):363-73 PubMed
Neurochem Res. 2003 Apr;28(3-4):499-506 PubMed
Exp Neurol. 2000 Feb;161(2):647-63 PubMed
Nat Rev Mol Cell Biol. 2000 Oct;1(1):31-9 PubMed
Int Rev Cytol. 1977;49:99-170 PubMed
J Physiol Paris. 2002 Jan-Mar;96(1-2):61-72 PubMed
Biochem J. 1969 Nov;115(3):465-72 PubMed
J Biol Chem. 1951 Nov;193(1):265-75 PubMed
J Biol Chem. 1994 Sep 2;269(35):21929-32 PubMed
Brain Res. 2000 Apr 17;862(1-2):180-6 PubMed
J Neurochem. 2003 Oct;87(2):297-309 PubMed
J Neurochem. 2002 Jan;80(1):178-90 PubMed