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Information:
Sphingosylphosphorylcholine (SPC), or lysosphingomyelin, is
a sphingolipid metabolite and putative second messenger important
in several intracellular and intercellular events and has
been implicated in regulation of cell growth, differentiation,
and programmed cell death. SPC increased intracellular calcium
concentration and nitric oxide production in endothelial cells
in situ causing endothelium-dependent vasorelaxation of bovine
coronary arteries.1 SPC also may regulate calcium
release from the sarcoplasmic reticulum by modifying the
gating kinetics of the cardiac ryanodine receptor.2
Stimulation of cardiac myocytes with SPC led to an increase
in the total amount of protein, an accelerated rate of total
protein synthesis, and a decrease in protein degradation, suggesting
that SPC may play a critical role in the development of cardiac
hypertrophy.3 Patients with atopic dermatitis
abnormally expressed sphingomyelin deacylase in their epidermis
resulting in elevated levels of SPC rather than ceramide. SPC
enhanced the expression of intercellular adhesion molecule-1
(ICAM-1), and transforming necrosis factor-alpha (TNF-alpha)
levels significantly increased in the medium of cultured human
keratinocytes. Also, SPC induced a rapid activation of mitogen-activated
protein kinase in keratinocytes. These finding suggest that
SPC plays an important role in the inflammatory process of epidermis
in skin diseases, such as atopic dermatitis, with high expression
of sphingomyelin deacylase.4 Finally, a study of
brain lipids in patients with the sphingomyelinase-deficient
types of Niemann-Pick disease demonstrated the abnormal accumulation
of SPC occurs only in the brain of neuronopathic type A patients
but not in the non-neuronopathic type B patients. Elevated
levels of SPC were observed in the brains of type A patients
while type B patients showed no significant increase of
SPC in brain lipids. Both type A and B patients exhibited abnormally
high levels of SPC in liver and spleen, establishing the integrity
of brain tissue in type B Niemann-Pick disease and suggesting
that SPC could play a role in the pathophysiology of brain dysfunction
in the neuronopathic type A.5
Source: Synthesized from D-erythro-Sphingosine Physical State: Powder Chemical Purity: >99%, by TLC and NMR.
References:
Mogami, K.; Mizukami, Y.; Todoroki-Ikeda, N.; Ohmura,
M.; Yoshida, K.; Miwa, S.; Matsuzaki, M.; Matsuda, M., and
Kobayashi, S. (1999 Sep 3). Sphingosylphosphorylcholine
induces cytosolic Ca2+ elevation in endothelial
cells in situ and causes endothelium-dependent relaxation
through nitric oxide production in bovine coronary artery.
FEBS Lett; 457(3):375-80.
Uehara, A.; Yasukochi, M.; Imanaga, I., and Berlin, J.
R. (1999 Nov 5). Effect of sphingosylphosphorylcholine on
the single channel gating properties of the cardiac ryanodine
receptor. FEBS Lett; 460(3):467-71.
Sekiguchi, K.; Yokoyama, T.; Kurabayashi, M.; Okajima,
F., and Nagai, R. (1999 Nov 26). Sphingosylphosphorylcholine
induces a hypertrophic growth response through the mitogen-activated
protein kinase signaling cascade in rat neonatal cardiac
myocytes. Circ Res; 85(11):1000-8.
Imokawa, G.; Takagi, Y.; Higuchi, K.; Kondo, H., and
Yada, Y. (1999 Jan). Sphingosylphosphorylcholine is a potent
inducer of intercellular adhesion molecule-1 expression
in human keratinocytes. J Invest Dermatol; 112(1):91-6.
Rodriguez-Lafrasse, C. and Vanier, M. T. (1999 Feb).
Sphingosylphosphorylcholine in Niemann-Pick disease brain:
accumulation in type A but not in type B. Neurochem Res;
24(2):199-205.