PMID- 9364332
OWN - NLM
STAT- MEDLINE
DCOM- 19980219
LR  - 20131121
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 50
IP  - 3
DP  - 1997 Nov 1
TI  - Myelin contains neutral sphingomyelinase activity that is stimulated by tumor 
      necrosis factor-alpha.
PG  - 466-76
AB  - Purified myelin from mouse brain was found to contain two forms of neutral 
      sphingomyelinase, one Mg2+ dependent and the other Mg2+ independent. The former 
      had a pH optimum of 7.5 and Km of 0.35 mM, whereas the corresponding values for 
      the latter were pH 8.0 and Km 3.03 mM. Specific activity of the Mg(2+)-dependent 
      enzyme showed a rostral-caudal gradient, ranging from 75 nmol/mg protein/hr in 
      myelin from cerebral hemispheres to 21 nmol/mg protein/hr in myelin from spinal 
      cord. Relative specific activity was approximately 20% that of brain stem or 
      cerebral hemisphere homogenate. Treatment of myelin with taurocholate or high 
      salt concentration did not significantly reduce activity of the Mg(2+)-dependent 
      enzyme. The activity of that enzyme did not change with time or in the presence 
      or absence of protease inhibitors; by contrast, that of Mg(2+)-independent enzyme 
      decreased sharply in the absence of protease inhibitors but rose in their 
      presence. To test for the effect of tumor necrosis factor-alpha (TNF alpha) on 
      myelin sphingomyelinase, mouse brain myelin was labeled in vivo by intracerebral 
      injection of [3H]acetate into 18-20-day-old mice. After 40 hr, brain stems were 
      removed, minced, and treated with TNF alpha in Krebs-Ringer solution, after which 
      myelin was immediately isolated. Separation and counting of individual lipids 
      revealed TNF alpha treatment to cause increased labeling of myelin ceramide and 
      cholesterol ester with concomitant decrease in myelin sphingomyelin. Western 
      blotting of myelin proteins using antibodies to the two TNF alpha receptors as 
      probes revealed the presence of the p75 receptor. Implications of these findings 
      in relation to possible mechanisms of autoimmune demyelination are discussed.
FAU - Chakraborty, G
AU  - Chakraborty G
AD  - Department of Neurosciences, New Jersey Medical School, Newark 07103, USA.
FAU - Ziemba, S
AU  - Ziemba S
FAU - Drivas, A
AU  - Drivas A
FAU - Ledeen, R W
AU  - Ledeen RW
LA  - eng
GR  - NS16181/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Acetates)
RN  - 0 (Ceramides)
RN  - 0 (Cholesterol Esters)
RN  - 0 (Diglycerides)
RN  - 0 (Isoenzymes)
RN  - 0 (Phosphatidylcholines)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.1.4.12 (Sphingomyelin Phosphodiesterase)
RN  - I38ZP9992A (Magnesium)
RN  - N91BDP6H0X (Choline)
SB  - IM
MH  - Acetates/metabolism
MH  - Animals
MH  - Brain/*enzymology
MH  - Brain Stem/enzymology
MH  - Cell Fractionation
MH  - Ceramides/metabolism
MH  - Cholesterol Esters/metabolism
MH  - Choline/metabolism
MH  - Diglycerides/metabolism
MH  - Isoenzymes/metabolism
MH  - Kinetics
MH  - Magnesium/pharmacology
MH  - Mice
MH  - Myelin Sheath/drug effects/*enzymology/metabolism
MH  - Phosphatidylcholines/metabolism
MH  - Sphingomyelin Phosphodiesterase/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1997/11/19 13:02
MHDA- 2000/06/20 09:00
CRDT- 1997/11/19 13:02
PHST- 1997/11/19 13:02 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/11/19 13:02 [entrez]
AID - 10.1002/(SICI)1097-4547(19971101)50:3<466::AID-JNR13>3.0.CO;2-4 [pii]
AID - 10.1002/(SICI)1097-4547(19971101)50:3<466::AID-JNR13>3.0.CO;2-4 [doi]
PST - ppublish
SO  - J Neurosci Res. 1997 Nov 1;50(3):466-76. doi: 
      10.1002/(SICI)1097-4547(19971101)50:3<466::AID-JNR13>3.0.CO;2-4.