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Comment
. 2014 Apr;63(4):1194-7.
doi: 10.2337/db14-0004.

Glycogen synthase kinase-3β and cathepsin B in diabetic endothelial progenitor cell dysfunction: an old player finds a new partner

Ranganath Muniyappa  1 , James R Sowers
Affiliations
Comment

Glycogen synthase kinase-3β and cathepsin B in diabetic endothelial progenitor cell dysfunction: an old player finds a new partner

Ranganath Muniyappa et al. Diabetes. 2014 Apr.
No abstract available

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Figures

Figure 1
Figure 1
GSK3β and cathepsin B in vasculogenesis. Endothelial injury and hypoxia activates HIF to initiate the expression and release of SDF-1, VEGF, c-Kit ligand (SCF), and IL-8. Circulating SDF-1 and VEGF stimulate the production of NO by endothelial NO synthase (eNOS) to MMP-9. Increased MMP-9 activity disrupts EPC-stromal cell interaction to mobilize EPCs from the marrow. Concentration gradients of SDF-1 direct circulating EPCs to the site of injury. Increased surface expression of integrin β2 and selectins (selectins E and P) on the endothelium interact with specific ligands on EPCs to recruit and home EPCs. In the unstimulated cell, GSK3β phosphorylates and accelerates the degradation of HIF-1α and β-catenin. Inhibition of GSK3β leads to nuclear translocation of HIF-1α and β-catenin. GSK3β inhibitors induce expression of cathepsin B to increase EPC proliferation and invasion. β Cat, β-catenin; DVL, disheveled; mSCF; membrane stem cell factor; PSGL-1, P-selectin glycoprotein ligand-1; sSCF, soluble SCF; LRP, low-density lipoprotein-related protein; VHL, von Hippel-Lindau protein; CXCR4, CXC chemokine receptor type 4; ICAM, intercellular adhesion molecule; and P, phosphorylation.
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