AI Article Synopsis
- Homeodomain proteins are crucial for developing the central nervous system and influence stem cell niches in the adult brain, particularly in the hippocampus.
- HOP (Homeodomain only protein) is expressed in radial astrocyte stem cells and regulates their survival; reducing HOP increases survival and promotes the formation of new neurons.
- In human glioblastomas, HOP is often absent, and restoring its function in glioma cells can induce cell death and decrease their ability to form tumors, indicating HOP’s potential as a tumor suppressor.
Article Abstract
Background: Homeodomain proteins play critical roles in shaping the development of the embryonic central nervous system in mammals. After birth, neurogenic activities are relegated to stem cell niches, which include the subgranular layer of the dentate gyrus of the hippocampus. Here, we have analyzed the function of HOP (Homeodomain only protein) in this stem cell niche and in human glioblastomas.
Results: We find that HOP is strongly expressed by radial astrocytes of the dentate gyrus in mice, which are stem cells that give rise to hippocampal granular neurons throughout adulthood. Deletion or down-regulation of HOP results in a decrease of apoptosis of these stem cells without changes in proliferation, and in an increase in the number of newly formed granule neurons. We also find that human glioblastomas largely lack HOP expression and that reintroduction of HOP function in glioma cells cultured as gliomaspheres leads to enhanced apoptosis in a subset of cases. In these cells, HOP function decreases clonogenicity.
Conclusion: These data suggest that HOP participates in the regulation of the adult mouse hippocampal stem cell niche by negatively affecting cell survival. In addition, HOP may work as a tumor suppressor in a subset of glioblastomas. HOP function thus appears to be critical in the adult brain in a region of continued plasticity, and its deregulation may contribute to disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2416439 | PMC |
| http://dx.doi.org/10.1186/1749-8104-3-13 | DOI Listing |
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