title: Stimulation of vascular cell proliferation by beta-galactoside specific lectins.
abstract: An investigation was conducted to assess the effects of various beta-galactoside specific lectins on the growth of vascular cells in vitro. The plant lectins from peanut (Arachis hypogaea), mushroom (Agaricus bisporus), and coral tree (Erythrina corallodendron) were used in these studies with the ultimate purpose of comparing those findings with data derived with the lectin isolated from rat lung. Peanut lectin was added to confluent and subconfluent cultures of smooth muscle cells (SMC), pulmonary arterial (PEC), and aortic endothelial cells (BAEC) at concentrations of 2, 3.5, and 7.0 micrograms/ml. There was a dose-dependent increase in cell proliferation for both confluent and subconfluent SMC, with maximal stimulation noted between 3.5 and 7 micrograms/ml of peanut lectin. A dose-dependent stimulation of PEC proliferation was also found with maximal stimulation between 3.5 and 7.0 micrograms/ml. Peanut lectin did not stimulate BAEC to multiply. The stimulation of PEC and SMC by peanut lectin could be prevented by the addition of 50 mM lactose. Peanut and mushroom lectin stimulated the proliferation of sparse cultures of SMC in a dose-dependent fashion in both standard (10% fetal bovine serum, or FBS) or low (0.5% FBS) serum to about the same degree. Coral tree lectin did not have a significant stimulation of proliferation under either serum conditions. The incorporation of [3H]thymidine into the DNA of PEC was increased 30 and 150% by peanut lectin and lung galaptin, respectively, under standard serum conditions. However, under low serum conditions, both lectins increased incorporation by about the same extent (93 and 78% for peanut lectin and galaptin, respectively). Both lectins produced a 30% increase in DNA synthesis by SMC under standard serum conditions, and about a 200% increase under low serum conditions. These studies indicate that beta-galactoside specific lectins such as lung galaptin have mitogenic activity toward vascular cells.
authors.affiliation: Department of Biochemistry, Morehouse School of Medicine, Atlanta, Georgia 30310.
authors.forename: G L
authors.initials: GL
authors.lastname: Sanford
authors.forename: S
authors.initials: S
authors.lastname: Harris-Hooker
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects; D010367:Arachis; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D004261:DNA Replication / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004895:Erythrina; D005697:Galactosides; D037161:Galectins; D006027:Glycosides; D006388:Hemagglutinins / Q000494:pharmacology*; D007700:Kinetics; D037102:Lectins / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000187:drug effects; D019887:Peanut Agglutinin; D037121:Plant Lectins; D010946:Plants, Medicinal; D013936:Thymidine / Q000378:metabolism
chemical_list: D005697:Galactosides; D037161:Galectins; D006027:Glycosides; D006388:Hemagglutinins; D037102:Lectins; D019887:Peanut Agglutinin; D037121:Plant Lectins; C045629:erythrina lectin; D013936:Thymidine