10.3389/fncel.2019.00023.s004
Hilal Celikkaya
Hilal
Celikkaya
Mehmet Ilyas Cosacak
Mehmet Ilyas
Cosacak
Christos Papadimitriou
Christos
Papadimitriou
Stanislava Popova
Stanislava
Popova
Prabesh Bhattarai
Prabesh
Bhattarai
Srijeeta Nag Biswas
Srijeeta Nag
Biswas
Tohid Siddiqui
Tohid
Siddiqui
Sabrina Wistorf
Sabrina
Wistorf
Isabel Nevado-Alcalde
Isabel
Nevado-Alcalde
Lisa Naumann
Lisa
Naumann
Violeta Mashkaryan
Violeta
Mashkaryan
Kerstin Brandt
Kerstin
Brandt
Uwe Freudenberg
Uwe
Freudenberg
Carsten Werner
Carsten
Werner
Caghan Kizil
Caghan
Kizil
Data_Sheet_4_GATA3 Promotes the Neural Progenitor State but Not Neurogenesis in 3D Traumatic Injury Model of Primary Human Cortical Astrocytes.ZIP
Frontiers
2019
GATA3
neurogenic potential
neural progenitors
scratch injury
primary human astrocytes
SOX2
2019-02-11 15:30:15
Dataset
https://frontiersin.figshare.com/articles/dataset/Data_Sheet_4_GATA3_Promotes_the_Neural_Progenitor_State_but_Not_Neurogenesis_in_3D_Traumatic_Injury_Model_of_Primary_Human_Cortical_Astrocytes_ZIP/7701362
<p>Astrocytes are abundant cell types in the vertebrate central nervous system and can act as neural stem cells in specialized niches where they constitutively generate new neurons. Outside the stem cell niches, however, these glial cells are not neurogenic. Although injuries in the mammalian central nervous system lead to profound proliferation of astrocytes, which cluster at the lesion site to form a gliotic scar, neurogenesis does not take place. Therefore, a plausible regenerative therapeutic option is to coax the endogenous reactive astrocytes to a pre-neurogenic progenitor state and use them as an endogenous reservoir for repair. However, little is known on the mechanisms that promote the neural progenitor state after injuries in humans. Gata3 was previously found to be a mechanism that zebrafish brain uses to injury-dependent induction of neural progenitors. However, the effects of GATA3 in human astrocytes after injury are not known. Therefore, in this report, we investigated how overexpression of GATA3 in primary human astrocytes would affect the neurogenic potential before and after injury in 2D and 3D cultures. We found that primary human astrocytes are unable to induce GATA3 after injury. Lentivirus-mediated overexpression of GATA3 significantly increased the number of GFAP/SOX2 double positive astrocytes and expression of pro-neural factor ASCL1, but failed to induce neurogenesis, suggesting that GATA3 is required for enhancing the neurogenic potential of primary human astrocytes and is not sufficient to induce neurogenesis alone.</p><p>HIGHLIGHTS-</p><p>Primary human astrocytes do not induce GATA3 after injury.</p>-<p>GATA3 promotes neural progenitor state but not neurogenesis.</p>-<p>GATA3 increases the GFAP/SOX2-positive cells and ASCL1 after injury in 3D.</p>-<p>GATA3 reduces lesion-induced scar-like collagen deposition.</p><p></p>