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Neutral sphingomyelinase: past, present and future.

S Chatterjee1

  • 1The Johns Hopkins Hospital, Baltimore, MD 21287-3654, USA. chatter@welchlink.welch.jhu.edu

Chemistry and Physics of Lipids
|September 23, 2000
PubMed
Summary
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Neutral sphingomyelinase (N-SMase) is crucial in cell signaling, producing ceramide that influences apoptosis and sterol regulation. Its activation by factors like TNF-alpha and Ox-LDL is implicated in atherosclerosis and may offer therapeutic targets.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Medicine

Background:

  • Sphingomyelinases (SMases) cleave sphingomyelin, producing ceramide, a key lipid second messenger involved in cellular signaling.
  • Ceramide regulates critical cellular processes including apoptosis, differentiation, proliferation, and sterol homeostasis.
  • Neutral sphingomyelinase (N-SMase) is activated by various stimuli, including tumor necrosis factor-alpha (TNF-alpha) and oxidized low-density lipoproteins (Ox-LDL).

Purpose of the Study:

  • To investigate the role of N-SMase and its product ceramide in cellular signaling pathways relevant to human diseases.
  • To explore the involvement of N-SMase activation in the pathogenesis of atherosclerosis.
  • To examine the differential effects of N-SMase activation on apoptosis and sterol regulation in different cell types.

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Main Methods:

  • Enzyme activity assays to measure N-SMase activation.
  • Cell culture experiments using human aortic smooth muscle cells and hepatocytes.
  • Treatment with TNF-alpha, Ox-LDL, and cell-permeable ceramide.
  • Assessment of apoptosis using antibody inhibition and overexpression studies.
  • Analysis of sterol regulatory element-binding protein (SREBP-1) maturation.

Main Results:

  • Ox-LDL and TNF-alpha stimulate N-SMase activity, leading to ceramide accumulation and apoptosis in vascular cells.
  • N-SMase activation is linked to plaque instability in atherosclerosis, with potential implications for stroke and heart failure.
  • In hepatocytes, TNF-alpha-mediated N-SMase activation promotes SREBP-1 maturation rather than apoptosis, suggesting cell-specific roles.
  • Overexpression of N-SMase in smooth muscle cells induces apoptosis, which can be abrogated by an N-SMase antibody.

Conclusions:

  • N-SMase plays significant, context-dependent cell regulatory roles in apoptosis and sterol metabolism.
  • N-SMase activation is a critical factor in atherosclerosis, potentially driving plaque rupture.
  • Targeting N-SMase offers a promising therapeutic strategy for hypercholesterolemia and atherosclerosis.