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Literature summary for 2.7.1.91 extracted from

  • Tauseef, M.; Kini, V.; Knezevic, N.; Brannan, M.; Ramchandaran, R.; Fyrst, H.; Saba, J.; Vogel, S.M.; Malik, A.B.; Mehta, D.
    Activation of sphingosine kinase-1 reverses the increase in lung vascular permeability through sphingosine-1-phosphate receptor signaling in endothelial cells (2008), Circ. Res., 103, 1164-1172.
    View publication on PubMedView publication on EuropePMC
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Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
lung
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 Mus musculus
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Expression

Organism Comment Expression
Mus musculus both lipopolysaccharide and thrombin increase mouse lung microvascular permeability and result in a delayed activation of SPHK1 that is coupled to the onset of restoration of pulmonary microvessel permeability down

General Information

General Information Comment Organism
physiological function in contrast to wild-type mice, Sphk1-/- mice show markedly enhanced pulmonary edema formation in response to lipopolysaccharide and PAR-1 activation. Increased SPHK1 activity and decreased intracellular S1P concentration precede the onset of lung microvascular barrier recovery. Knockdown of SPHK1 decreases basal sphingosine 1-phoshate production and Rac1 activity but increases basal endothelial permeability. In SPHK1-depleted cells, PAR-1 activation fails to induce Rac1 activation but augments RhoA activation and endothelial hyperpermeability response. Knockdown of S1P1 receptor in endothelial cells also enhances the increase in endothelial permeability following PAR-1 activation. Sphingosine 1-phosphate treatment of Sphk1-/- lungs or SPHK1-deficient endothelial cells restores endothelial barrier function Mus musculus