The retina represents an ideal model system for studying developmental processes during morphogenesis. The knowledge of the precise regulation and combination of genetic pre-dispositions and environmental circumstances enables the understanding of pathologies and the subsequent development or/and improvement of therapeutic strategies. This study focused on the functional analysis of the extracellular matrix (ECM) molecule Tenascin C (Tnc) in the retinal stem/progenitor cell environment. In this perspective, a Tnc(-/-) mouse was examined for potential alterations in proliferation and differentiation programs by using immunohistochemistry, RT-PCR analysis and bioassays. It could be shown that both cycling G2-phase cells and early post-mitotic neurons were significantly increased in the retina due to Tnc-deficiency. Further investigations suggested that Tnc regulates these processes via the Wnt-signaling cascade. Therapeutic approaches in the treatment of degenerative diseases often integrate cell-replacement strategies. Retinal Müller glia cells represent the glia of the retina and are described to possess the ability to re-enter the cell cycle and generate neurons in response to injury. In this study, the de-differentiation was induced by FGF2. It was found out that Tnc influences the de-differentiation behavior of adherent Müller glia in vitro. Moreover, it was interesting to investigate the effect of the absence of Tnc on the composition of other components of the ECM. A special focus lay on the expression of a specifically sulfated carbohydrate motif on chondroitin sulfate glycosaminoglycan chains, which can be detected with the mAb 473HD. It was possible to note a significant increase of this particular chondroitin sulfate in the Tnc-deficient ECM.
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