targeting of demyelinated lesions in experimental models of multiple sclerosis using a fibrin binding peptide

Introduction: multiple sclerosis (ms) is an autoimmune and inflammatory disease of the central nervous system characterized by demyelination, astrogliosis, blood-brain barrier (bbb) disruption, and axonal damage. currently available clinical and experimental approaches for ms are not completely effective because of the inability to pass the bbb, off-target distribution, and the need to increase the dosage. it has been shown that bbb disruption and fibrin deposition occur in the region of lesions in ms. coagulation factor xiii binds to fibrin through the heptapeptide nqeqvsp in its structure. here, nqeqvsp was used to target the lesions in animal models of ms. methods: microglia, astrocytes, and oligodendrocytes were immuno- stained using antibodies against iba1, gfap, and mbp, respectively.results: we showed that peptide nqeqvsp binding was specific to the lesion sites induced by lysophosphatidylcholine (lpc) injection into the corpora callosa of mice. the peptide was fam labeled, and its co-localization with different glial cells was evaluated. co-localization was mainly detected with the microglia in the damaged area. a lower level of co-localization was also observed for oligodendrocytes.conclusion: our results promise the possibility of using nqeqvsp peptide to target the lesions for specific drug delivery in patients suffering from multiple sclerosis.