| Literature DB >> 20974670 |
Yun-Bi Lu1, Ianors Iandiev, Margrit Hollborn, Nicole Körber, Elke Ulbricht, Petra G Hirrlinger, Thomas Pannicke, Er-Qing Wei, Andreas Bringmann, Hartwig Wolburg, Ulrika Wilhelmsson, Milos Pekny, Peter Wiedemann, Andreas Reichenbach, Josef A Käs.
Abstract
Increased stiffness of reactive glial cells may impede neurite growth and contribute to the poor regenerative capabilities of the mammalian central nervous system. We induced reactive gliosis in rodent retina by ischemia-reperfusion and assessed intermediate filament (IF) expression and the viscoelastic properties of dissociated single glial cells in wild-type mice, mice lacking glial fibrillary acidic protein and vimentin (GFAP(-/-)Vim(-/-)) in which glial cells are consequently devoid of IFs, and normal Long-Evans rats. In response to ischemia-reperfusion, glial cells stiffened significantly in wild-type mice and rats but were unchanged in GFAP(-/-)Vim(-/-) mice. Cell stiffness (elastic modulus) correlated with the density of IFs. These results support the hypothesis that rigid glial scars impair nerve regeneration and that IFs are important determinants of cellular viscoelasticity in reactive glia. Thus, therapeutic suppression of IF up-regulation in reactive glial cells may facilitate neuroregeneration.Entities:
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Year: 2010 PMID: 20974670 DOI: 10.1096/fj.10-163790
Source DB: PubMed Journal: FASEB J ISSN: 0892-6638 Impact factor: 5.191