Stimulation of vascular cell proliferation by β‐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.

Upregulation of galectin-7 in murine lymphoma cells is associated with progression toward an aggressive phenotype

“…The members of the galectin family have been reported to participate in several lymphomagenesis-associated processes. Indeed, galectins have been shown to (1) promote the adhesion of lymphoma cells to vascular EC, 47 (2) promote the proliferation of endothelial cells, 48 (3) induce apoptosis in T leukemia cell lines, 49 (4) mediate homotypic adhesion of tumor cells, 50 and (5) protect tumor cells from Fas-induced apoptosis. 51 Moreover, levels of galectins are elevated in many neoplastic diseases, including lymphomas, in the cases of galectin-3.…”

Stimulation of Proliferation of Rat Hepatic Stellate Cells by Galectin-1 and Galectin-3 through Different Intracellular Signaling Pathways

“…Galectin-1 and galectin-3 are present intracellularly (both in the cytoplasm and the nucleus), extracellularly, and at the cell surface (10 -14). Galectin-1 and galectin-3 play roles in cell proliferation (15)(16)(17), differentiation (18,19), adhesion (20, 21), neoplastic transformation (22,23), and apoptosis (24 -26), and in the interaction of neoplastic cells with ECMs (27)(28)(29). Over such a wide range of influences, galectins are thought to modulate cell signaling by cross-linking with target molecules through their ␤-galactoside-containing glycoconjugates (30,31).…”

Overexpression of α1-protease Inhibitor and Galectin-1 in Radiation-induced Early Phase of Pulmonary Fibrosis

“…Galectin-1 forms a homodimer of 14 kDa subunits, which play roles in cell proliferation, differentiation, and apoptosis. In addition, they promote the proliferation of rat pulmonary arterial endothelial cells and vascular smooth muscle cells via binding between the β-galactosidecontaining moieties of their cell surface receptor (18). Therefore, some galectin subtypes might be used as a good disease marker of pulmonary fibrosis.…”