Fig. 1.
Fig. 1. Sickle RBCs adhere to laminin. A 1% hematocrit of sickle (SS) RBCs or normal (AA) RBCs was flowed across immobilized protein (0.75 μg). Adherent cells from four representative regions were counted by microscopy, normalized to cells per square millimeter, and shown as the mean ± SD. (A) Significant adhesion of sickle, but not normal, RBCs was observed to human laminin (hLAM). Only background levels of adhesion were observed with sickle RBCs to the negative control BSA. Data from 10 sickle cell patients are shown. (B) Sickle RBCs were flowed across immobilized recombinant human entactin (ENT) or collagen IV (Coll IV). SS RBCs did not adhere to either entactin or collagen IV. BSA and hLAM are shown as negative and positive controls, respectively. Data from 3 patients are shown. (C) Immobilized hLAM was pretreated with an antilaminin polyclonal antibody (pAb) before the introduction of the SS 1% hematocrit. The antilaminin pAb significantly inhibited the adhesion of sickle RBCs to hLAM. Adhesion to laminin in the absence of an antibody (hLAM) and in the presence of a nonspecific, isotype-matched IgG antibody are shown as negative controls. Data shown represent experiments from 4 patients.

Sickle RBCs adhere to laminin. A 1% hematocrit of sickle (SS) RBCs or normal (AA) RBCs was flowed across immobilized protein (0.75 μg). Adherent cells from four representative regions were counted by microscopy, normalized to cells per square millimeter, and shown as the mean ± SD. (A) Significant adhesion of sickle, but not normal, RBCs was observed to human laminin (hLAM). Only background levels of adhesion were observed with sickle RBCs to the negative control BSA. Data from 10 sickle cell patients are shown. (B) Sickle RBCs were flowed across immobilized recombinant human entactin (ENT) or collagen IV (Coll IV). SS RBCs did not adhere to either entactin or collagen IV. BSA and hLAM are shown as negative and positive controls, respectively. Data from 3 patients are shown. (C) Immobilized hLAM was pretreated with an antilaminin polyclonal antibody (pAb) before the introduction of the SS 1% hematocrit. The antilaminin pAb significantly inhibited the adhesion of sickle RBCs to hLAM. Adhesion to laminin in the absence of an antibody (hLAM) and in the presence of a nonspecific, isotype-matched IgG antibody are shown as negative controls. Data shown represent experiments from 4 patients.

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