Uses
Plasminogen is a single-chain glycoprotein found in human plasma and extracellular fluid. Certain activators, such as tissue plasminogen activator (tPA), convert plasminogen to its active form, plasmin. Plasminogen has been used to study its conversion into plasmin.
General Description
The plasminogen (PLG) gene is mapped to human chromosome 6q26. Plasminogen protein has a molecular weight of 90kDa. It is composed of Pan-apple domain at the N-terminal, five kringle domains and serine protease domain at its C-terminal.
Biochem/physiol Actions
Plasminogen is the inactive precursor of the protease plasmin. Plasminogen is activated by the action of either tissue plasminogen activator (tPA), which primarily activates the fibrinolytic (thrombolytic) activity of plasmin, or urokinase plasminogen activator (uPA), which is associated with extracellular matrix remodeling and cell migration. Plasmin cleaves fibrin/fibrinogen and blood coagulation factors V/Va and VIII/VIIIa. It activates matrix metalloproteinases by cleaving the inactive proenzymes. It is also involved in the activation of some growth factors, such as vascular endothelial growth factor (VEGF) and transforming growth factor β (TGF-β).
in vivo
Plasminogen (plg) (2 mg/per; i.v.; single daily for 16 days) accelerates the healing of burn wounds in WT mice[1].
Plasminogen (plg) (2 mg/per; i.v.; single daily for 16 days) enhances the expression of IL-6 and augments the activation of STAT3 in wounded skin of both WT and plg-deficient mice[1].
Plasminogen (plg) (2 mg/per; i.v.; single daily for 24 days) improves the healing of burn wounds in a mouse model of diabetes[1].
| Animal Model: | WT mice (plg-heterozygous (plg+/-)) mice, plg+/- and plg-deficient (plg-/-) mice (C57BL/6 background; 8- to 10- week-old; burn-wound model)[1]. |
| Dosage: | 2 mg/per |
| Administration: | Intravenous injection; single daily for 16 days. |
| Result: | Showed a significantly faster healing speed than control group at day 6, and the time to healing (ie, the scab falling off) was also approximately 2 days earlier than in the control group.
Promoted epithelium layer fused to reepithelialize the wound completely, and only a small scab remained lightly attached above the wound when at day 11.
Enhanced the level of IL-6 in the wounds of both WT and plg-deficient mice, and increased the pSTA T3 level in the wound.
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| Animal Model: | Genetically diabetic mice (C57BLKS db/db; at least 10 weeks old; with a minimal blood glucose level of 15 mM) and control heterozygous littermates (C57BLKS db/+; at least 10 weeks old; with a minimal blood glucose level of 7.8 mM)[1]. |
| Dosage: | 2 mg/per |
| Administration: | Intravenous injection; single daily for 24 days. |
| Result: | Showed time to healing (ie, the scab falling off) was significantly earlier (approximately 3 days) than the control group.
Accelerated the injured epithelium layer and the underlying tissue healed. (the front of the epithelium layer in the control group had barely fused and was covered by a scab. In addition, the tissue underneath the scab was inflamed).
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