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Synemin is expressed in reactive astrocytes in neurotrauma and interacts differentially with vimentin and GFAP intermediate filament networks

Artikel i vetenskaplig tidskrift
Författare R. Jing
Ulrika Wilhelmsson
W. Goodwill
Lizhen Li
Y. Pan
Milos Pekny
O. Skalli
Publicerad i J Cell Sci
Volym 120
Nummer/häfte Pt 7
Sidor 1267-77
ISSN 0021-9533 (Print)
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 1267-77
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Neurobiologi

Sammanfattning

Immature astrocytes and astrocytoma cells contain synemin and three other intermediate filament (IF) proteins: glial fibrillary acidic protein (GFAP), vimentin and nestin. Here, we show that, after neurotrauma, reactive astrocytes produce synemin and thus propose synemin as a new marker of reactive astrocytes. Comparison of synemin mRNA and protein levels in brain tissues and astrocyte cultures from wild-type, Vim(-)(/)(-) and Gfap(-)(/)(-)Vim(-)(/)(-) mice showed that in the absence of vimentin, synemin protein was undetectable although synemin mRNA was present at wild-type levels. By contrast, in Gfap(-)(/)(-) astrocytes, synemin protein and mRNA levels, as well as synemin incorporation into vimentin IFs, were unaltered. Biochemical assays with purified proteins suggested that synemin interacts with GFAP IFs like an IF-associated protein rather than like a polymerization partner, whereas the opposite was true for synemin interaction with vimentin. In transfection experiments, synemin did not incorporate into normal, filamentous GFAP networks, but integrated into vimentin and GFAP heteropolymeric networks. Thus, alongside GFAP, vimentin and nestin, reactive astrocytes contain synemin, whose accumulation is suppressed post-transcriptionally in the absence of a polymerization partner. In astrocytes, this partner is vimentin and not GFAP, which implies a functional difference between these two type III IF proteins.

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