does it more than simply attract monocytes?
MCP-1 does not only exhibit direct effects on tubular epithelial cells, but also on another cell type that plays a role in progressive renal damage, i.e. vascular smooth muscle cells [22]. Stimulation of vascular smooth muscle cells with MCP-1 induced proliferation and resulted in a concentration- and time-dependent release of IL-6. Similar to tubular epithelial cells, this effect was mediated via Gi-protein, PKC and NF-B. MCP-1 also induced extracellular signal-regulated kinase (ERK), which, along with IL-6 release, was Gi-protein-dependent. MCP-1-induced, proliferation of vascular smooth muscle cells, which was ERK-dependent. MCP-1 stimulated the binding activity of NF-B and of AP-1. NF-B was involved in IL-6 release by MCP-1, whereas proliferation was dependent on AP-1, demonstrating that, as in tubular epithelial cells, MCP-1 induces differential activation of NF-B and AP-1 in vascular smooth muscle cells. Thus, these latter data do not only propose a new mechanism for the proather
