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Updated: Aug 3, 2026

Ex Vivo Imaging of Postnatal Cerebellar Granule Cell Migration Using Confocal Macroscopy
Published on: May 12, 2015
Secretion of plasminogen activator by human polymorphonuclear leukocytes. Modulation by glucocorticoids and other
Abstract:
Purified human PMNs secrete plasminogen activator. This secretion is stimulated by Con A and low concentrations of PMA, and is inhibited by low concentrations of glucocorticoids, and by cAMP, actinomycin D, and cycloheximide. In contrast, the release of granule-bound enzymes, such as elastase, is achieved only at higher concentrations of PMA, and is not affected by any of the inhibitors that block plasminogen activator production. These results show that the production of plasminogen activatory by PMNs is controlled by agents that affect inflammations, and that this control is not shared by other lytic enzymes known to be associated with these cells. This suggests a particular role for plasminogen activator in the response pattern of PMNs and also supports the concept, previously developed for macrophages, that the secretion of this enzyme is correlated with cell migration in vivo.
Insights
Human neutrophils (PMNs) secrete plasminogen activator, a process regulated by inflammation-affecting agents and distinct from other lytic enzyme release, suggesting a role in cell migration.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Human polymorphonuclear neutrophils (PMNs) are key immune cells involved in inflammatory responses.
- The secretion of specific enzymes by PMNs plays a crucial role in their function and interaction with tissues.
- Plasminogen activator is an enzyme secreted by various cells, involved in fibrinolysis and extracellular matrix remodeling.
Purpose of the Study:
- To investigate the regulation of plasminogen activator secretion by human PMNs.
- To compare the regulatory mechanisms of plasminogen activator production with those of other granule-bound enzymes, such as elastase.
- To explore the potential role of plasminogen activator secretion in PMN inflammatory responses and cell migration.
Main Methods:
- Purification of human PMNs.
- Stimulation of PMN secretion using Concanavalin A (Con A) and phorbol 12-myristate 13-acetate (PMA) at varying concentrations.
- Inhibition studies using glucocorticoids, cyclic adenosine monophosphate (cAMP), actinomycin D, and cycloheximide.
- Assay of plasminogen activator and elastase release.
Main Results:
- Plasminogen activator secretion by PMNs is stimulated by Con A and low concentrations of PMA.
- Glucocorticoids, cAMP, actinomycin D, and cycloheximide inhibit plasminogen activator production.
- Release of granule-bound elastase requires higher PMA concentrations and is unaffected by the inhibitors that block plasminogen activator production.
Conclusions:
- PMN plasminogen activator production is distinctly regulated by agents influencing inflammation, separate from other lytic enzymes like elastase.
- The specific control mechanisms suggest a unique role for plasminogen activator in the PMN response pattern.
- Findings support the hypothesis that plasminogen activator secretion correlates with cell migration in vivo, similar to observations in macrophages.
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