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Characterization of the role of Sphk2 in pancreatic beta cells
Author(s) -
Cantrell Jamie,
Özcan Sabire
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a293-d
Subject(s) - sphingosine kinase , sphingosine , beta cell , sphingosine kinase 1 , microbiology and biotechnology , chemistry , biology , medicine , endocrinology , sphingosine 1 phosphate , insulin , biochemistry , receptor , islet
The pancreatic beta cells are responsible for making and releasing the hormone insulin in response to high blood glucose levels. Insulin stimulates glucose uptake from the blood into the muscle and adipose tissues. Diabetes is the result of beta cell death, insulin resistance, and beta cell dysfunction. We are interested in glucose‐regulated beta cell function. DNA microarray data was collected on the expression of genes in mouse insulonoma cells (MIN6) at both low (1mM) and high (25mM) glucose conditions. One gene in particular, Sphingosine kinase 2 (Sphk2), was shown to have approximately a 3‐fold increase in expression on low glucose. Sphingosine‐1‐phosphate (S1P) is the product of Sphingosine kinase (Sphk) activity. There are two known isoforms of this enzyme referred to as Sphk1 and Sphk2. S1P is a lipid molecule involved in numerous signal transduction pathways. However, the cell signaling activities of Sphk are still under speculation. Sphk2 has been reported to be involved in cell viability. Since Sphk2 expression is increased on low glucose (based on DNA microarray data), we hypothesize that Sphk2 is involved in protecting beta cells from apoptosis in the absence of glucose. We will test this hypothesis, by performing overexpression and knockdown studies of Sphk2 in beta cells and thereby determine its role in beta‐cell viability.