Trypanosoma evansi impacts on embryonic neural progenitor cell functions

Fracasso, Mateus; Pillat, Micheli Mainardi; Bottari, Nathieli B.; Silva, Aniélen D. da; Grando, Thirssa H.; Matos, Antônio Francisco Igor Magalhães de; Petry, Letícia S.; Ulrich, Henning; Andrade, Cínthia Melazzo de; Monteiro, Sílvia González; Silva, Aleksandro S. Da

doi:10.1016/j.micpath.2019.103703

Cited by 1 publication

(1 citation statement)

References 24 publications

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“…Nevertheless, the manipulation of these signaling cascades does not lead to the full recovery of NSC neurogenic potential ( He et al, 2009 , Martens et al, 2002 , Seaberg et al, 2005 , Whittemore et al, 1999 ). Understanding the mechanisms that regulate neurogenesis in vivo, can lead to the design of new therapies to promote neural repair after injury (as reviewed by Ruddy and Morshead (2018) ) or treatment for pathologies that impair the functioning of NSC during development, like parasitic infections ( Bottari et al, 2019 , Fracasso et al, 2019 ). Many of these studies have focus on the telencephalic NSC, in this work we focus on the differentiation potential of the spinal cord because of the biomedical relevance of this tissue.…”

Section: Introductionmentioning

confidence: 99%

Proliferation rate and differentiation potential are independent during the transition from neurogenesis to gliogenesis in the mouse embryonic spinal cord

Olivos-Cisneros

Ramı́rez-Santos

Gutiérrez‐Ospina

2021

IBRO Neuroscience Reports

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Neural stem cells (NSC) restrict their differentiation potential as the central nervous system develops. Experimental evidence suggests that the mechanisms governing the transition from the neurogenic to the gliogenic phase irreversibly affect the ability of NSC to generate neurons. Cell cycle regulation has been associated with cell fate in different models. In this work, we assessed the temporal correlation between the loss of the neurogenic potential and cell cycle lengthening of NSC obtained from embryonic mouse spinal cords, during the transition of the neurogenic to the gliogenic phase, using neurospheres. We also used the cell cycle inhibitor Olomoucine to increase cell cycle length by decreasing the proliferation rate. Our results show that neurospheres obtained from a neurogenic stage give rise mostly to neurons, whereas those obtained from later stages produce preferentially glial cells. During the transition from neurogenesis to gliogenesis, the proliferation rate dropped, and the cell cycle length increased 1.5 folds, as monitored by DNA BrdU incorporation. Interestingly, Olomoucine-treated neurogenic-neurospheres display a reduced proliferation rate and preserve their neurogenic potential. Our results suggest that the mechanisms that restrict the differentiation potential of NSC are independent of the proliferation control.

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