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These studies suggest a crucial role for peripheral PL in mediating neuroimmune cell activation and Alzheimer's disease (AD) progression and could provide a link to systemic inflammatory risk factors that are known to be associated with AD development.
Variation in blood plasminogen levels, within the range seen in normal individuals, had marked effects on experimental ischemic brain injury
plasmin protease activity prevents dystrophic calcification within injured skeletal muscle independent of its canonical fibrinolytic function.
Plasminogen-deficient mice have extensive fibrin and neutrophil depositions in the wounded area long after re-epithelialisation, indicating inefficient debridement and chronic inflammation. Delayed formation of granulation tissue suggests that fibroblast function is impaired in the absence of plasminogen.
confirmed the ability of Plg/Pla to both promote efferocytosis and override the prosurvival effect of LPS via annexin A1.
findings identify plasmin as a decisive checkpoint in the inflammatory response during Macrophage activation syndrome (MAS) and a potential novel therapeutic target for MAS.
Deficiency of plasminogen delays onset of autoimmune neuroinflammatory disease and protects from the development of paralysis.
Plasminogen may regulate DPP-4 activity and glucose metabolism.
Plasminogen-deficient mice frequently develop colon lesions and rectal prolapses.
manganese transport protein C (MntC) is an extracellular matrix- and plasminogen-binding protein
Plg from mouse plasma contains oxPtdPC adducts that are not affected by the action of Lp-PLA(2), suggesting that linkage to Plg protects oxPtdPCs from metabolism during their transport in the plasma.
plg-/- and tPA-/- mice exhibit brain parenchymal fibrin deposits that appear to result from reduced neurovascular integrity
plasminogen-dependent proteolysis has a beneficial effect during neurological recovery after stroke.
Pla-induced mononuclear cell recruitment in vivo was dependent on protease-activated receptor-1 activation of the MEK/ERK/NF-kappaB pathway, which led to the release of CCL2 and activation of CCR2.
Plg may play an important role in innate immunity by changing expression of genes that contribute to phagocytosis.
Plasminogen is a key molecular determinant of inflammatory joint disease capable of simultaneously driving or ameliorating arthritis pathogenesis in distinct anatomic locations in the same subject.
Plasmin suppresses brain metastasis in two ways: by converting membrane-bound astrocytic FasL into a paracrine death signal for cancer cells, and by inactivating the axon pathfinding molecule L1CAM, which metastatic cells express for spreading along brain capillaries and for metastatic outgrowth.
Plasminogen stimulates autocrine cytokine production in human airway smooth muscle cells in a manner mediated by plasmin and annexin A2.
plasminogen contributes to angiogenesis related to macrophage accumulation, TGF-beta, and VEGF, thereby leading to the enhancement of bone repair.
These findings highlight a critical role for plasmin in the catabolism of aggregated LDL by macrophages and provide a new context for considering the atherogenic role of plasmin.
Angiostatin is an angiogenesis inhibitor that blocks neovascularization and growth of experimental primary and metastatic tumors in vivo. Plasmin dissolves the fibrin of blood clots and acts as a proteolytic factor in a variety of other processes including embryonic development, tissue remodeling, tumor invasion, and inflammation. In ovulation, weakens the walls of the Graafian follicle. It activates the urokinase-type plasminogen activator, collagenases and several complement zymogens, such as C1 and C5. Cleavage of fibronectin and laminin leads to cell detachment and apoptosis. Also cleaves fibrin, thrombospondin and von Willebrand factor. Its role in tissue remodeling and tumor invasion may be modulated by CSPG4. Binds to cells (By similarity).
, plasmin heavy chain A
, plasmin light chain B