Citation

Mouse Neural Stem/Progenitor Response to Neonatal Hypoxia/Ischemia and the Role of Leukemia Inhibitory Factor

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Abstract:

According to the World Health Organization, permanent neurological disorders affect up 1 billion people worldwide, causing shortened lifespan and deterioration in quality of life. To alleviate these problems, different neurorestorative strategies have been considered. This study focuses on stimulating the expansion of endogenous neural stem cells (NSCs) for term infant brain repair. The subventricular zone (SVZ) is the discrete region within the brain that harbors neural stem and progenitor cells (NSPs) during and after the development of the nervous system has ceased. These NSPs rely on extracellular signals produced by cells within and lining the lateral ventricles, that promote their ability to self-renew, to expand and to a limited extent, determines their fate. Expanding the numbers of resident stem offers new opportunities for treating brain injuries. This research focuses on neonatal hypoxia/ischemia (H/I), the major cause of permanent neurological disabilities sustained during childhood that has an annual incidence of over 120,000 infants in the US and presently has no treatment. The aim of this study was to determine whether there is an increase in NSPs after neonatal H/I, whether Leukemia Inhibitory Factor (LIF) increases in the mouse SVZ after injury, and to establish how LIF affects NSP homeostasis. Our data reveal an amplification of the NSPs 2-4 days after H/I, as evidenced by increased Ki67+/nestin+/musashi-1+ cells in the most medial aspect of the SVZ of the injured hemisphere compared to the contralateral SVZ. This increase in NSPs is preceeded by an increase in LIF mRNA. LIF mRNA is rapidly induced but only for 48 hours by Q-PCR. We have established that astrocytes, but not microglia or NSPs release LIF. Upon harvesting the SVZ 3 days after neonatal H/I, the neurosphere assay revealed an increase in number and size of primary neurospheres in the injured SVZ compared to controls. Upon differentiation, there was more than twice as many tri-potential neurospheres from the damaged brain compared to controls. However, there was no increase in 2° neurospheres. Stimulating NSPs with rhLIF chronically for 10 days, decreased expansion and neurosphere size at doses from 10-20 ng/ml, while at 2-5 ng/ml rhLIF increased NSP growth. These data demonstrate that neonatal H/I increases the abundance of mouse neural stem cells commensurate with an increase in LIF, which exerts concentration dependent effects on mouse NSPs homeostasis.
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Association:
Name: Connecticut's Stem Cell Research International Symposium
URL:
http://stemconn.org


Citation:
URL: http://citation.allacademic.com/meta/p365859_index.html
Direct Link:
HTML Code:

MLA Citation:

Buono, Krista., Jiang, Yuhui. and Levison, Steve. "Mouse Neural Stem/Progenitor Response to Neonatal Hypoxia/Ischemia and the Role of Leukemia Inhibitory Factor" Paper presented at the annual meeting of the Connecticut's Stem Cell Research International Symposium, Omni Hotel, New Haven, CT, Mar 23, 2009 <Not Available>. 2014-11-29 <http://citation.allacademic.com/meta/p365859_index.html>

APA Citation:

Buono, K. D., Jiang, Y. and Levison, S. W. , 2009-03-23 "Mouse Neural Stem/Progenitor Response to Neonatal Hypoxia/Ischemia and the Role of Leukemia Inhibitory Factor" Paper presented at the annual meeting of the Connecticut's Stem Cell Research International Symposium, Omni Hotel, New Haven, CT <Not Available>. 2014-11-29 from http://citation.allacademic.com/meta/p365859_index.html

Publication Type: Poster
Review Method: Peer Reviewed
Abstract: According to the World Health Organization, permanent neurological disorders affect up 1 billion people worldwide, causing shortened lifespan and deterioration in quality of life. To alleviate these problems, different neurorestorative strategies have been considered. This study focuses on stimulating the expansion of endogenous neural stem cells (NSCs) for term infant brain repair. The subventricular zone (SVZ) is the discrete region within the brain that harbors neural stem and progenitor cells (NSPs) during and after the development of the nervous system has ceased. These NSPs rely on extracellular signals produced by cells within and lining the lateral ventricles, that promote their ability to self-renew, to expand and to a limited extent, determines their fate. Expanding the numbers of resident stem offers new opportunities for treating brain injuries. This research focuses on neonatal hypoxia/ischemia (H/I), the major cause of permanent neurological disabilities sustained during childhood that has an annual incidence of over 120,000 infants in the US and presently has no treatment. The aim of this study was to determine whether there is an increase in NSPs after neonatal H/I, whether Leukemia Inhibitory Factor (LIF) increases in the mouse SVZ after injury, and to establish how LIF affects NSP homeostasis. Our data reveal an amplification of the NSPs 2-4 days after H/I, as evidenced by increased Ki67+/nestin+/musashi-1+ cells in the most medial aspect of the SVZ of the injured hemisphere compared to the contralateral SVZ. This increase in NSPs is preceeded by an increase in LIF mRNA. LIF mRNA is rapidly induced but only for 48 hours by Q-PCR. We have established that astrocytes, but not microglia or NSPs release LIF. Upon harvesting the SVZ 3 days after neonatal H/I, the neurosphere assay revealed an increase in number and size of primary neurospheres in the injured SVZ compared to controls. Upon differentiation, there was more than twice as many tri-potential neurospheres from the damaged brain compared to controls. However, there was no increase in 2° neurospheres. Stimulating NSPs with rhLIF chronically for 10 days, decreased expansion and neurosphere size at doses from 10-20 ng/ml, while at 2-5 ng/ml rhLIF increased NSP growth. These data demonstrate that neonatal H/I increases the abundance of mouse neural stem cells commensurate with an increase in LIF, which exerts concentration dependent effects on mouse NSPs homeostasis.


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