Abstract
The stem cell source of neural and glial progenitors in the periventricular regions of the adult forebrain has remained uncertain and controversial. Using a cell specific genetic approach we rule out Foxj1+ ependymal cells as stem cells participating in neurogenesis and gliogenesis in response to acute injury or stroke in the mouse forebrain. Non stem- and progenitor-like responses of Foxj1+ ependymal cells to injury and stroke remain to be defined and investigated.
Highlights
Past reports have suggested that adult ependymal cells (ECs), or a subpopulation thereof, have endogenous stem cell potential with the ability to generate new neurons for the olfactory bulbs (OBs) and in response to stroke in the mouse forebrain
Concerned that the human promoter element utilized in the past studies (a ~ 1 kb upstream human FOXJ1 locus) was resulting in ectopic expression patterns, we generated a knock-in Foxj1creERT2::GFP mouse to lineage-trace potential EC progeny from the endogenous locus
Our results indicate minimal, if any, direct cellular contribution from the Foxj1+ ependymal cell pool to sites of insult or other forebrain regions after injury and stroke
Summary
Past reports have suggested that adult ependymal cells (ECs), or a subpopulation thereof, have endogenous stem cell potential with the ability to generate new neurons for the olfactory bulbs (OBs) and in response to stroke in the mouse forebrain. Concerned that the human promoter element utilized in the past studies (a ~ 1 kb upstream human FOXJ1 locus) was resulting in ectopic expression patterns, we generated a knock-in Foxj1creERT2::GFP mouse to lineage-trace potential EC progeny from the endogenous locus. This line has been characterized[8] and was used in a recent study illustrating that spinal cord injury fails to induce Foxj1+ ECs to proliferate or to substantially contribute new cells to the glial scar[9]. To test the possibility that damage or stroke in the forebrain may contribute to the reported transformation of ependyma into neurogenic or gliogenic progenitors, a stab injury and three distinct stroke models were employed
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