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Maile, L.A. et al.

Laura A. Maile, Lee B. Allen, Christopher F. Hanzaker, Katherine A. Gollahon, Paul Dunbar, David R. Clemmons,

Glucose regulation of thrombospondin and its role in the modulation of smooth muscle cell proliferation.

Smooth muscle cells (SMC) maintained in high glucose are more responsive to IGF-I than those in normal glucose. There is significantly more thrombospondin-1 (TSP-1) in extracellular matrix surrounding SMC grown in 25 mM glucose. In this study we investigated 1) the mechanism by which glucose regulates TSP-1 levels and 2) the mechanism by which TS-1 enhances IGF-I signaling. The addition of TSP-1 to primary SMC was sufficient to enhance IGF-I responsiveness in normal glucose. Reducing TSP-1 protein levels inhibited IGF-I signaling in SMC maintained in high glucose. We determined that TSP-1 protected IAP/CD47 from cleavage and thereby facilitated its association with SHP substrate-1 (SHPS-1). We have shown previously that the hyperglycemia induced protection of IAP from cleavage is an important component of the ability of hyperglycemia to enhance IGF-I signaling. Furthermore we determined that TSP-1 also enhanced phosphorylation of the beta3 subunit of the alphaVbeta3 integrin, another molecular event that we have shown are critical for SMC response to IGF-I in high glucose. Our studies also revealed that the difference in the amount of TSP-1 in the two different glucose conditions was due, at least in part, to a difference in the cellular uptake and degradation of TSP-1.[1]

References

Glucose regulation of thrombospondin and its role in the modulation of smooth muscle cell proliferation. Maile, L.A., Allen, L.B., Hanzaker, C.F., Gollahon, K.A., Dunbar, P., Clemmons, D.R. Exp. Diabetes. Res (2010) [Pubmed]

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