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Literature summary for 2.7.1.91 extracted from

  • Takuwa, N.; Ohkura, S.; Takashima, S.; Ohtani, K.; Okamoto, Y.; Tanaka, T.; Hirano, K.; Usui, S.; Wang, F.; Du, W.; Yoshioka, K.; Banno, Y.; Sasaki, M.; Ichi, I.; Okamura, M.; Sugimoto, N.; Mizugishi, K.; Nakanuma, Y.; Ishii, I.; Takamura, M.; Kaneko, S.; Kojo, S.; Satouchi, K.; Mitumori, K.; Chun, J.; Takuwa Y.
    S1P3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species (2010), Cardiovasc. Res., 85, 484-493.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine chronic activation of SPHK1-S1P signalling results in both pathological cardiac remodelling through reactive oxygen species mediated by S1P3 and favourable cardioprotective effects Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining

General Information

General Information Comment Organism
physiological function SPHK1-transgenic mice overexpress SPHK1 in diverse tissues, with a nearly 20fold increase in enzymatic activity. The transgenic mice grow normally with normal blood chemistry, cell counts, heart rate, and blood pressure. Transgenic mice with high but not low expression levels of SPHK1 develop progressive myocardial degeneration and fibrosis, with upregulation of embryonic genes, elevated RhoA and Rac1 activity, stimulation of Smad3 phosphorylation, and increased levels of oxidative stress markers. Treatment of juvenile transgenic mice with pitavastatin, or deletion of S1P3, a major myocardial S1P receptor subtype both inhibit cardiac fibrosis with concomitant inhibition of SPHK1-dependent Smad-3 phosphorylation. In addition, the anti-oxidant N-2-mercaptopropyonylglycine, also inhibits cardiac fibrosis. In in vivo ischaemia/reperfusion injury, the size of myocardial infarct is 30% decreased in SPHK1-transgenic mice compared with wild-type mice Mus musculus