TY - JOUR
T1 - Vascular differentiation and glucose transporter expression in rat gliomas
T2 - Effects of steroids
AU - Guerin, Christopher
AU - Wolff, Johannes E.A.
AU - Laterra, John
AU - Drewes, Lester R.
AU - Brem, Henry
AU - Goldstein, Gary W.
PY - 1992/5
Y1 - 1992/5
N2 - The GLUT1 isoform of the glucose transporter is normally expressed at high levels in differentiated brain vessels that also express a permeability barrier. In contrast, malignant brain neoplasms have relatively undifferentiated vessels that are highly permeable, proliferate to high vascular densities, and often lose GLUT1 expression. Using the rat intracerebral 9L glioma model, we investigated whether dexamethasone‐induced changes in permeability are associated with the appearance of other differentiated vascular properties. The percentage of vessels expressing immunohistochemically detectable GLUT1 (74.2 ± 6.1%) and the tumor vessel density as assessed by laminin immunostaining (282 ± 37 vessels/mm2) did not vary with control tumor size. Dexamethasone treatment resulted in an 83% reduction of vascular permeability to intravenous Evans blue, an increased percentage of vessels expressing GLUT1 (106.4 ± 10.5%), lower vascular density (102 ± 64 vessels/mm2), and smaller tumor size (control cross‐sectional area, 17.0 ± 3.4 mm2; treated, 4.6 ± 1.0 mm2). Essentially all vessels became GLUT1‐positive after dexamethasone treatment. Increased GLUT1 expression by glioma vessels in association with the appearance of other signs of differentiation (low vascular density, slow tumor growth) suggests that immunostaining for GLUT1 may identify neoplasms that are biologically less aggressive.
AB - The GLUT1 isoform of the glucose transporter is normally expressed at high levels in differentiated brain vessels that also express a permeability barrier. In contrast, malignant brain neoplasms have relatively undifferentiated vessels that are highly permeable, proliferate to high vascular densities, and often lose GLUT1 expression. Using the rat intracerebral 9L glioma model, we investigated whether dexamethasone‐induced changes in permeability are associated with the appearance of other differentiated vascular properties. The percentage of vessels expressing immunohistochemically detectable GLUT1 (74.2 ± 6.1%) and the tumor vessel density as assessed by laminin immunostaining (282 ± 37 vessels/mm2) did not vary with control tumor size. Dexamethasone treatment resulted in an 83% reduction of vascular permeability to intravenous Evans blue, an increased percentage of vessels expressing GLUT1 (106.4 ± 10.5%), lower vascular density (102 ± 64 vessels/mm2), and smaller tumor size (control cross‐sectional area, 17.0 ± 3.4 mm2; treated, 4.6 ± 1.0 mm2). Essentially all vessels became GLUT1‐positive after dexamethasone treatment. Increased GLUT1 expression by glioma vessels in association with the appearance of other signs of differentiation (low vascular density, slow tumor growth) suggests that immunostaining for GLUT1 may identify neoplasms that are biologically less aggressive.
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U2 - 10.1002/ana.410310504
DO - 10.1002/ana.410310504
M3 - Article
C2 - 1596083
AN - SCOPUS:0026568675
SN - 0364-5134
VL - 31
SP - 481
EP - 487
JO - Annals of neurology
JF - Annals of neurology
IS - 5
ER -