![]() ![]() Some of these secreted proteins play important roles in the progression of inflammatory diseases in the brain, and serve as biomarkers that can be used to guide diagnosis and drug therapy. Secretomic analysis has been previously conducted for astrocytes and microglia to determine the profile of the secreted proteins. This may have important implications in the regulation of brain microglial activities in health and disease.Īctivated glial cells secrete a variety of proteins including proinflammatory cytokines, chemokines, and neurotoxic factors under inflammatory or pathological conditions. Our results indicate that glia-derived PAI-1 may regulate microglial migration and phagocytosis in an autocrine or paracrine manner. PAI-1 inhibited microglial engulfment of zymosan particles in a vitronectin- and Toll-like receptor 2/6-dependent manner. Moreover, PAI-1 was able to modulate microglial phagocytic activity. PAI-1-mediated microglial migration was independent of protease inhibition, because an R346A mutant of PAI-1 with impaired PA inhibitory activity also promoted microglial migration. PAI-1 also increased microglial migration in vivo when injected into mouse brain. PAI-1 promoted the migration of microglial cells in culture via the low-density lipoprotein receptor-related protein (LRP) 1/Janus kinase (JAK)/signal transducer and activator of transcription (STAT)1 axis. The levels of PAI-1 mRNA and protein expression were increased by lipopolysaccharide and interferon-γ stimulation in both microglia and astrocytes. Phagocytic activity was measured by uptake of zymosan particles. Cell migration was evaluated by in vitro scratch-wound healing assay or Boyden chamber assay and an in vivo stab wound injury model. Secretion of PAI-1 from glial cultures was detected by ELISA and western blotting analysis. In this study, we identified PAI-1 in the culture medium of mouse mixed glial cells by liquid chromatography and tandem mass spectrometry. However, little is known about the role of PAI-1 in the central nervous system. PAI-1 is also involved in the innate immunity by regulating cell migration and phagocytosis. It aims also to describe the gradual arrest of their motility much of which occurs within a few minutes.Plasminogen activator inhibitor type 1 (PAI-1) is the primary inhibitor of urokinase type plasminogen activators (uPA) and tissue type plasminogen activators (tPA), which mediate fibrinolysis. This review of the published data explains the present understanding of physico-chemical mechanisms by which flagellar motility is activated (mostly through osmotic and ionic regulation) and then propels sperm cells at speed. Their specific inability to restore their energy content (mostly adenosine triphosphate) fast enough relatively to their high rate of energy consumption by flagellar contributes mainly to the activity arrest of motility, as the spermatozoa need to rely on early accumulated energy prior to activation. Their flagella immediately develop waves propagated at high beat frequency (up to 70 beats s −1), which propel these sperm cells at high velocity (6–10 mm min −1), but for a quite short period of time, usually limited to minutes. ![]() In most species, fish spermatozoa activate their motility on contact with the external medium (sea or fresh water depending of their reproductive habitat). ![]()
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