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. 2009 Jun;11(3):260–273. doi: 10.1215/15228517-2008-094

Fig. 3.

Fig. 3

Glioma adhesion correlates with glutamate receptor type 1 (GluR1) expression. (A and B) Glioma cells were plated on 96-well plates precoated with type I collagen (Col I), type IV collagen (Col IV), fibronectin (FN), or vitronectin (VN). Adhesion to both type I and type IV collagen in U251 (A) and U87 (B) cells was significant in controls compared to short hairpin GluR1 (shGluR1; *) and in GluR1-overexpressing (**) cells compared to controls. White columns, shGluR1 cells; black columns, control cells; cross-hatched columns, GluR1-overexpressing cells. (C) Adhesion of U87 and U251 glioma cells overexpressing GluR1 was dependent on β1 integrin. BSA, bovine serum albumin (negative control); IgG, immunoglobulin G (positive control). (D) α-Amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor (AMPAR) stimulation reduced adhesion of glioma cells to collagen. Glioma cells were stimulated with serum-free media (control, hatched bars), 50 μM AMPA (checkered bars), 100 μM AMPA alone (horizontal-striped bars), or AMPAR desensitization inhibitor cyclothiazide (vertical-striped bars) after plating onto collagen. *, ** p < 0.05, Student’s t-test, for C and D. Results are expressed as mean ± SEM. Experiments were conducted in triplicate.