Table 2.
Histopathological evidence of fibrinolytic pathway components in multiple sclerosis.
| Fibrinolytic components | Main findings (patient sample size/methodology) | References |
|---|---|---|
| Fibrinolysis | Higher fibrinolytic activity in plaques than adjacent NAWM. | (115) |
| tPA | Staining for infiltrated mononuclear cells in MS lesions and WM. Strong positivity of foamy macrophages in areas of demyelination and decline in chronic lesions. | (116) |
| Co-localization with non-phosphorylated neurofilament and fibrin deposition in demyelinated axons. | (67) | |
| Decreased tPA activity in acute MS lesions. Decreased fibrinolytic activity in demyelinating MS plaques due to tPA/PAI-1 complex. | (117) | |
| tPA receptors | Localization on macrophages, astrocytes. Increased in MS lesions compared to NAWM. | (118) |
| uPA, uPAR | Detected in acute MS lesions, expressed by mononuclear cells in perivascular cuffs and to macrophages in the lesion parenchyma. uPAR additionally detected in NAWM. | (67) |
| D-dimers | Localization on foamy macrophages and demyelinating axons. | (117) |
| PAI-1 | Detected in acute MS lesions, expressed by mononuclear cells in perivascular cuffs and to macrophages in the lesion parenchyma. | (67) |
| Up-regulation in progressive MS cortex but without an efficient fibrin degradation (immunohistochemistry on the cortex of 47 progressive MS and 10 controls). | (12) |
NAWM, normal-appearing white matter; MS, multiple sclerosis; PAI-1, plasminogen activator inhibitor 1; tPA, tissue-type plasminogen activator; uPAR, urokinase plasminogen activator receptor; WM, white matter.