Oligodendrocyte progenitor proliferation is disinhibited following traumatic brain injury in leukemia inhibitory factor heterozygous mice

2021 ◽  
Author(s):  
Michelle J. Frondelli ◽  
Marie L. Mather ◽  
Steven W. Levison
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor ◽  
Oligodendrocyte Progenitor

Leukemia Inhibitory Factor Is Expressed in Astrocytes Following Cortical Brain Injury

1997 ◽  
Vol 147 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Lisa R. Banner ◽  
N.Nicole Moayeri ◽  
Paul H. Patterson
Keyword(s):  
Brain Injury ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor

scholarly journals Human Traumatic Brain Injury Results in Oligodendrocyte Death and Increases the Number of Oligodendrocyte Progenitor Cells

2016 ◽  
Vol 75 (6) ◽  
pp. 503-515 ◽  
Author(s):  
Johanna Flygt ◽  
Astrid Gumucio ◽  
Martin Ingelsson ◽  
Karin Skoglund ◽  
Jonatan Holm ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Progenitor Cells ◽  
Oligodendrocyte Progenitor Cells ◽  
Oligodendrocyte Progenitor

scholarly journals Oligodendrocyte progenitor proliferation is disinhibited following traumatic brain injury in LIF heterozygous mice

2020 ◽  
Author(s):  
Michelle J. Frondelli ◽  
Marie. L. Mather ◽  
Steven W. Levison
Keyword(s):  
Traumatic Brain Injury ◽  
Cell Proliferation ◽  
Brain Injury ◽  
Progenitor Cell ◽  
Closed Head Injury ◽  
Normal Brain ◽  
List Type ◽  
Color Flow ◽  
Oligodendrocyte Progenitor ◽  
Progenitor Cell Proliferation

AbstractTraumatic brain injury (TBI) is a significant problem that affects ∼500,000 children each year. As cell proliferation is disturbed by injury and is required for normal brain development, we investigated how a pediatric closed head injury (CHI) would affect the progenitors of the subventricular zone (SVZ). Additionally, we evaluated the contribution of Leukemia Inhibitory Factor (LIF) using LIF-heterozygous mice (LIF Het), as LIF is an injury-induced cytokine, known to influence neurogenesis and gliogenesis. CHI’s were performed on P20 LIF Het and WT mice. Ki-67 staining and stereology revealed that cell proliferation increased ∼250% in injured LIF Het mice compared to the 30% increase observed in injured WT mice at 48 h post CHI. Furthermore, Olig2+ cell proliferation increased in the SVZ and white matter of LIF Het injured mice at 48 h recovery. Using an 8-color flow cytometry panel, the proliferation of three distinct multipotential progenitors were greater in LIF Het injured mice compared to WT injured mice. Early oligodendrocyte progenitor cell (OPC) proliferation was 6-fold higher in LIF Het injured mice compared to WT injured mice. In vitro, addition of LIF decreased overall cell proliferation and OPC proliferation compared to controls. Addition of LIF to OPC cultures induced an increase of phospho-Akt after 20 minutes and an increase of phospho-S6RP at 20 and 40 minutes of exposure, suggesting that LIF stimulates the mammalian target of Rapamycin pathway. Altogether, our data provide new insights into the regulatory role of LIF in suppressing neural progenitor cell proliferation after a mild TBI.Main PointsOPC proliferation is dis-inhibited in LIF haplodeficient mice.LIF directly inhibits glial progenitor cell proliferation.LIF stimulates the mTOR pathway.

Leukemia Inhibitory Factor Haplodeficiency Desynchronizes Glial Reactivity and Exacerbates Damage and Functional Deficits after a Concussive Brain Injury

2016 ◽  
Vol 33 (16) ◽  
pp. 1522-1534 ◽  
Author(s):  
Matthew T. Goodus ◽  
Nadine A. Kerr ◽  
Ruchika Talwar ◽  
David Buziashvili ◽  
Jennifer E.C. Fragale ◽  
...  
Keyword(s):  
Brain Injury ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor ◽  
Functional Deficits ◽  
Glial Reactivity

scholarly journals Neuroregenerative and protective functions of Leukemia Inhibitory Factor in perinatal hypoxic-ischemic brain injury

2020 ◽  
Vol 330 ◽  
pp. 113324
Author(s):  
Jie Lin ◽  
Yusuke Niimi ◽  
Mariano Guardia Clausi ◽  
Hur Dolunay Kanal ◽  
Steven W. Levison
Keyword(s):  
Brain Injury ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Activation of Cytokine Signaling through Leukemia Inhibitory Factor Receptor (LIFR)/gp130 Attenuates Ischemic Brain Injury in Rats

2005 ◽  
Vol 25 (6) ◽  
pp. 685-693 ◽  
Author(s):  
Shigeaki Suzuki ◽  
Toru Yamashita ◽  
Kortaro Tanaka ◽  
Hidenori Hattori ◽  
Kazunobu Sawamoto ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
Leukemia Inhibitory Factor ◽  
Inhibitory Factor ◽  
Cytokine Signaling ◽  
Ischemic Damage ◽  
Ischemic Brain Injury ◽  
Leukemia Inhibitory Factor Receptor ◽  
Ischemic Brain ◽  
Phosphorylated Stat3

Cytokine signaling through leukemia inhibitory factor receptor (LIFR)/gp130 is known to exert a neurotrophic action in the central nervous system, although the role of this signaling in cerebral ischemia remains unknown. We examined the effect of intracerebral injection of LIF after focal cerebral ischemia in rats. The animals underwent a sham operation (sham group) or middle cerebral artery occlusion (MCAO) followed by direct injection of either vehicle (phosphate-buffered saline, the PBS group) or recombinant LIF (10 ng in the low-LIF group and 100 ng in the high-LIF group) into the cerebral cortex adjacent to the inner boundary zone of the infarct area, and neurologic and histologic evaluations were conducted 24 h later. Expression of LIFR, gp130, and phosphorylated Stat3, Akt, and ERK1/2 was investigated by Western blot analysis and immunohistochemistry. The neurologic deficits and ischemic damage were significantly less severe in the high-LIF group than in the PBS group and the low-LIF group. Leukemia inhibitory factor receptor and gp130 were expressed in neurons, and the ischemic damage of these proteins was rescued in the high-LIF group. Early induction of phosphorylated Stat3 was significantly detected on the ischemic side in the high-LIF group after LIF injection. Exogenous LIF attenuates ischemic brain injury by activating cytokine signaling through LIFR/gp130.

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