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Macrophage Stimulating Protein/Chemokine (MSP/CCL-16) and Induction of Cell Cycle Activity by Heparin.
In a previous report we demonstrated a potential heparin-induced cell cycle arrest of tumor cells through the induction of cdc2 kinase activity. In this report, we characterized the structure of macrophage stimulating protein (MSP)/CCL-16, a heparin-binding chemokine, and investigated the possibility of cell cycle arrest of human tumor cells by MSP, as well as the effect of heparin. Heparin was found to bind to purified MSP/CCL-16 in vitro. Culture supernatants of various heparin-treated human cell lines were evaluated for the ability to support the growth of a receptor positive, heparin-specific cell line. The supernatants were found to support the growth of the target cells in a dose-dependent manner, which was only found to be inhibited by the addition of anti-MSP/CCL-16 monoclonal antibody. In a semiquantitative competition assay, supernatants of tumor cells, which had been incubated in the presence of heparin, were found to significantly inhibit the binding of 125I-MSP/CCL-16 to its receptor. However, heparin alone or under similar experimental conditions did not stimulate the proliferation of receptor positive human tumor cells, indicating that MSP/CCL-16 alone did not appear to be responsible for heparin-induced cell cycle arrest.namespace EventStore.ClientAPI {
using System.Collections.Generic;
using System.Linq;
using EventStore.Common.Utils;
using EventStore.ClientAPI.Exceptions;

public interface IEventReaderComponent {
EventSeriesInfo GetEventSeriesInfo(Guid uid);

/// Get an instance for the specified and a new one if the one for the current component is not available.


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