Contributions
Abstract: EP1499
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms
Astrocytes are impressive versatile cells and seem to have functions in driving inflammation as well as in facilitating remyelination dependent on their immediate plaque milieu by expressing a variety of mediators. How astrocytes intervene and what forces them to act in the one or other way is still poorly understood, making astrocytes an interesting research aim. In our previous work we investigated the astrocytic reaction in experimental autoimmune encephalomyelitis in Dark Agouti rats by correlating glial scar reaction with the presence of oligodendrocyte precursor cell over the full course of lesion evolution up to a successfully completed remyelination. We furthermore investigated remyelination facilitating factors adumbrating a beneficial role of astrocytes during the remyelinating process. We assume that at least in our investigated animal model an abundant glial scar reaction does not prohibit remyelination.
To further characterise the astrocytic involvement during destruction and repair we investigated the following remyelination inhibiting factors expressed by astrocytes: Hyaluronan, Tenascin C and Fibronectin 1. All of them are suggested in literature to substantially contribute to remyelination failure. We performed immunohistochemical double staining of those factors and GFAP to find co-localisations in our sample set. Quantitative evaluation and statistical analysis were performed for all lesion stages in a total of 300 lesions so far.
In comparison to the remyelination facilitating factors, where most of them reached their peak during early remyelination process, the maximum of remyelination inhibiting factors were found during active demyelination. Preliminary data show that over 80 % of all GFAP positive cells in actively demyelinating lesions were carrying Hyaluronan binding protein 2 on their surface. In comparison approximately 50 % of GFAP positive cells in active lesions were carrying Fibronectin 1 and Tenascin C respectively.
There is evidence that there are different phenotypes of astrocytes correlated to their facilitating or prohibiting function on remyelination. In our further research we want to correlate A1 and A2 astrocytic phenotypes to the investigated remyelination facilitating and prohibiting factors expressed by astrocytes in all lesion stages of our animal model. Our work aims to describe astrocytic involvement from active demyelinating lesions up to successful repair in this animal model of Multiple Sclerosis.
Disclosure: Haindl: nothing to disclose
Köck: nothing to disclose
Zeitelhofer-Adzemovic: nothing to disclose
Fazekas: nothing to disclose
Hochmeister: nothing to disclose
Abstract: EP1499
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Repairing mechanisms
Astrocytes are impressive versatile cells and seem to have functions in driving inflammation as well as in facilitating remyelination dependent on their immediate plaque milieu by expressing a variety of mediators. How astrocytes intervene and what forces them to act in the one or other way is still poorly understood, making astrocytes an interesting research aim. In our previous work we investigated the astrocytic reaction in experimental autoimmune encephalomyelitis in Dark Agouti rats by correlating glial scar reaction with the presence of oligodendrocyte precursor cell over the full course of lesion evolution up to a successfully completed remyelination. We furthermore investigated remyelination facilitating factors adumbrating a beneficial role of astrocytes during the remyelinating process. We assume that at least in our investigated animal model an abundant glial scar reaction does not prohibit remyelination.
To further characterise the astrocytic involvement during destruction and repair we investigated the following remyelination inhibiting factors expressed by astrocytes: Hyaluronan, Tenascin C and Fibronectin 1. All of them are suggested in literature to substantially contribute to remyelination failure. We performed immunohistochemical double staining of those factors and GFAP to find co-localisations in our sample set. Quantitative evaluation and statistical analysis were performed for all lesion stages in a total of 300 lesions so far.
In comparison to the remyelination facilitating factors, where most of them reached their peak during early remyelination process, the maximum of remyelination inhibiting factors were found during active demyelination. Preliminary data show that over 80 % of all GFAP positive cells in actively demyelinating lesions were carrying Hyaluronan binding protein 2 on their surface. In comparison approximately 50 % of GFAP positive cells in active lesions were carrying Fibronectin 1 and Tenascin C respectively.
There is evidence that there are different phenotypes of astrocytes correlated to their facilitating or prohibiting function on remyelination. In our further research we want to correlate A1 and A2 astrocytic phenotypes to the investigated remyelination facilitating and prohibiting factors expressed by astrocytes in all lesion stages of our animal model. Our work aims to describe astrocytic involvement from active demyelinating lesions up to successful repair in this animal model of Multiple Sclerosis.
Disclosure: Haindl: nothing to disclose
Köck: nothing to disclose
Zeitelhofer-Adzemovic: nothing to disclose
Fazekas: nothing to disclose
Hochmeister: nothing to disclose