Mesangial cell migration precedes proliferation in Habu snake venom-induced glomerular injury.

Background: Mesangial cells migrate in response to platelet released products in vitro (Am J Pathol 1991;138:859). Cell migration, in addition to proliferation might play a role in cell remodeling during the course of proliferative glomerular disease.

Experimental Design: In this study, we examined mesangial cell migration in vivo in a platelet-dependent model of proliferative glomerulonephritis induced by Habu snake venom.

Extrarenal cytokines modulate the glomerular response to IgA immune complexes.

Clinical episodes of IgA nephropathy coincide recurrently with microbial infections. Cytokines produced during such infections may play a role in the pathogenesis of IgA-associated glomerulonephritis. To test this hypothesis, we examined the influence of passively administered proinflammatory cytokines (IL-1, IFN-gamma and IL-6) on the development of glomerulonephritis in an experimental model of IgA nephropathy.

Glomerular mesangial cell migration. Response to platelet secretory products.

Glomerular mesangial cells migrate in response to platelet-derived growth factor (PDGF), but to date these cells have not been examined for migratory behavior in response to other platelet secretory products. Because migration might provide an additional mode of cell redistribution and local mesangial hypercellularity in certain forms of glomerular disease, we examined, in vitro, the potential of isolated rat mesangial cells to migrate toward gradients of platelet releasate and selected platelet secretory proteins. Chemotaxis assays were performed in two compartment blind well chambers, each compartment separated by a porous membrane.

Glomerular mesangial cell migration in response to platelet-derived growth factor.

Platelet-derived growth factor (PDGF) is a potent mitogenic and chemotactic protein for a variety of cell types. Glomerular mesangial cells also respond to PDGF in terms of proliferation, but, to date, have not been examined for migratory behavior in response to a specific growth factor. Here, we examine the ability of isolated rat mesangial cells to migrate toward gradients of purified PDGF.

Hepatocyte cell surface polarity as demonstrated by lectin binding.

We performed an investigation at the ultrastructural level of the differential distribution of lectin-binding sites among sinusoidal, lateral, and bile canalicular domains of adult rat hepatocytes. Lectin binding to hepatocyte glycocalices was studied in situ or after cellular dissociation by enzymatic (collagenase), chemical (EDTA), and mechanical methods, as well as during cell culture. Using thirteen biotinylated lectins and an avidin-biotin-peroxidase complex (ABC), we have identified lectin-binding sites that are predominantly localized in the bile canalicular [Ricinus communis agglutinin (RCA)] or sinusoidal [Phaseolus vulgaris (PHA)] domains in situ and in mechanically dissociated cells.