2007
DOI: 10.1016/j.cardiores.2007.01.015
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Deletion of the Sphingosine Kinase-1 gene influences cell fate during hypoxia and glucose deprivation in adult mouse cardiomyocytes

Abstract: As the effect of GM-1 is blocked both at the receptor and the G-protein (Gi) levels, we conclude that S1P generated by GM-1 treatment must be exported from the cell and acts in a paracrine or autocrine manner to couple with its cognate receptor.

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Cited by 76 publications
(75 citation statements)
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References 33 publications
(53 reference statements)
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“…Accumulating evidence has implicated the S1P metabolism in hypoxia in normal cells. Indeed, we and others have shown the involvement of SphK1 in the adaptation of cardiomyocytes to ischemia both in vitro and in animal models (11,12), and SphK1-null cardiomyocytes have been shown to be more susceptible to hypoxia (13). Moreover, increased proliferation of smooth muscle cells induced by hypoxia relies on the generation of S1P (14), and increased SphK1 expression was reported in pulmonary smooth muscle cells under both acute and chronic hypoxia (15).…”
Section: Introductionmentioning
confidence: 80%
“…Accumulating evidence has implicated the S1P metabolism in hypoxia in normal cells. Indeed, we and others have shown the involvement of SphK1 in the adaptation of cardiomyocytes to ischemia both in vitro and in animal models (11,12), and SphK1-null cardiomyocytes have been shown to be more susceptible to hypoxia (13). Moreover, increased proliferation of smooth muscle cells induced by hypoxia relies on the generation of S1P (14), and increased SphK1 expression was reported in pulmonary smooth muscle cells under both acute and chronic hypoxia (15).…”
Section: Introductionmentioning
confidence: 80%
“…In culture, S1P reduced apoptosis in mesoangioblasts and in cardiac cells (Donati et al, 2007). Tao et al (2007) found that decreased S1P synthesis reduced cell survival. Neutralisation of S1P with a monoclonal antibody blocked in vivo angiogenesis induced by fibroblast growth factor and VEGF (Argraves et al, 2010).…”
Section: Discussionmentioning
confidence: 98%
“…Additionally, a connection has been hypothesized between the SphK1/S1P metabolism and hypoxia based on the SphK1-dependent vascular smooth muscle cell growth increase under acute hypoxic stress (33) and the transcriptional mediated SphK1 expression in pulmonary smooth muscle cells under both acute and chronic hypoxia (34). More recently, SphK1-null cardiomyocytes have been shown to be more susceptible to hypoxia and glucose deprivation (35). A single article has recently suggested a link between SphK1 and CoCl 2 chemically induced hypoxia in cancer cells (36).…”
Section: Discussionmentioning
confidence: 99%