References of "Worlitzer, Maik M. A."
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailThe majority of newly generated cells in the adult mouse substantia nigra express low levels of Doublecortin, but their proliferation is unaffected by 6-OHDA-induced nigral lesion or Minocycline-mediated inhibition of neuroinflammation.
Worlitzer, Maik M. A.; Viel, Thomas; Jacobs, Andreas H. et al

in European Journal of Neuroscience (2013)

Parkinson's disease is characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN). However, whether regenerative endogenous neurogenesis is taking place in the mammalian SN of ... [more ▼]

Parkinson's disease is characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN). However, whether regenerative endogenous neurogenesis is taking place in the mammalian SN of parkinsonian and non-parkinsonian brains remains of debate. Here, we tested whether proliferating cells in the SN and their neurogenic potential would be affected by anti-inflammatory treatment under physiological conditions and in the 6-hydroxy-dopamine (6-OHDA) Parkinson's disease mouse model. We report that the majority of newly generated nigral cells are positive for Doublecortin (Dcx), which is an often used marker for neural progenitor cells. Yet, Dcx expression levels in these cells were much lower than in neural progenitor cells of the subventricular zone and the dentate gyrus neural progenitor cells. Furthermore, these newly generated nigral cells are negative for neuronal lineage markers such as TuJ1 and NeuN. Therefore, their neuronal commitment is questionable. Instead, we found evidence for oligodendrogenesis and astrogliosis in the SN. Finally, neither short-term nor long-term inhibition of neuroinflammation by Minocycline- or 6-OHDA-induced lesion affected the numbers of newly generated cells in our disease paradigm. Our findings of adult generated Dcx+ cells in the SN add important data for understanding the cellular composition and consequently the regenerative capacity of the SN. [less ▲]

Detailed reference viewed: 174 (7 UL)
Full Text
Peer Reviewed
See detailJAM-C is an apical surface marker for neural stem cells.
Stelzer, Sandra; Worlitzer, Maik M. A.; Bahnassawy, Lamia A et al

in Stem Cells & Development (2012), 21(5), 757-66

Junctional adhesion molecule-C (JAM-C) is an adhesive cell surface protein expressed in various cell types. JAM-C localizes to the apically localized tight junctions (TJs) between contacting endothelial ... [more ▼]

Junctional adhesion molecule-C (JAM-C) is an adhesive cell surface protein expressed in various cell types. JAM-C localizes to the apically localized tight junctions (TJs) between contacting endothelial and epithelial cells, where it contributes to cell-cell adhesions. Just as those epithelial cells, also neural stem cells are highly polarized along their apical-basal axis. The defining feature of all stem cells, including neural stem cells (NSCs) is their ability to self renew. This self-renewal depends on the tight control of symmetric and asymmetric cell divisions. In NSCs, the decision whether a division is symmetric or asymmetric largely depends on the distribution of the apical membrane and cell fate determinants on the basal pole of the cell. In this study we demonstrate that JAM-C is expressed on neural progenitor cells and neural stem cells in the embryonic as well as the adult mouse brain. Furthermore, we demonstrate that in vivo JAM-C shows enrichment at the apical surface and therefore is asymmetrically distributed during cell divisions. These results define JAM-C as a novel surface marker for neural stem cells. [less ▲]

Detailed reference viewed: 157 (2 UL)
Full Text
Peer Reviewed
See detailNeural stem cells maintain their stemness through protein kinase C zeta-mediated inhibition of TRIM32.
Hillje, Anna-Lena; Worlitzer, Maik M. A.; Palm, Thomas et al

in Stem Cells (2011), 29(9), 1437-47

Several studies over the last couple of years have delivered insights into the mechanisms that drive neuronal differentiation. However, the mechanisms that ensure the maintenance of stemness ... [more ▼]

Several studies over the last couple of years have delivered insights into the mechanisms that drive neuronal differentiation. However, the mechanisms that ensure the maintenance of stemness characteristics in neural stem cells over several rounds of cell divisions are still largely unknown. Here, we provide evidence that the neuronal fate determinant TRIM32 binds to the protein kinase C zeta. Through this interaction, TRIM32 is retained in the cytoplasm. However, during differentiation, this interaction is abrogated and TRIM32 translocates to the nucleus to initiate neuronal differentiation by targeting c-Myc for proteasomal degradation. [less ▲]

Detailed reference viewed: 126 (4 UL)