Treatment with Minocycline Suppresses Microglia Activation and Reverses Neural Stem Cells Loss after Simulated Microgravity

The present study aimed to investigate the effect of microglia on simulated microgravity-induced hippocampal neurogenesis reduction and the possible mechanism underlying. Adult rats were treated with tail suspension for different times and the changes of neural stem cells (NSCs) were examined by immunohistochemistry. Then, minocycline was used to inhibit the activation of microglia, and the numbers of microglia and NSCs were detected after microgravity. Additionally, liquid protein chip analysis was applied to detect proinflammatory factors in hippocampus in order to find out the cytokines responsible for microglia activation after microgravity. The results revealed that microgravity increased the numbers of Iba1+ cells and decreased the numbers of BrdU+ and DCX+ cells in hippocampus but did not affect the ratio of NeuN+/BrdU+ cells to the total number of BrdU+ cells. After treated with minocycline, activated microglia were suppressed and the reduction of NSCs induced by microgravity recovered. Besides, compared with the control, higher concentrations of INF-γ and TNF-α were detected in the rats treated with microgravity. Our study provides the first evidence that microglia-mediated inflammation plays an important part in microgravity-induced neurogenesis reduction in hippocampus, and INF-γ and TNF-α secreted by microglia might be the key factors in this process.

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Systematic Review of Nicotine Exposure’s Effects on Neural Stem and Progenitor Cells

Brain Sciences ◽

10.3390/brainsci11020172 ◽

2021 ◽

Vol 11 (2) ◽

pp. 172

Author(s):

Arrin C. Brooks ◽

Brandon J. Henderson

Keyword(s):

Stem Cells ◽

Neural Stem Cells ◽

Inverse Correlation ◽

Hippocampal Neurogenesis ◽

Nicotine Exposure ◽

Negative Consequences ◽

Postnatal Neurogenesis ◽

Cognitive Behaviors ◽

Chronic Nicotine ◽

Stem And Progenitor Cells

While various modalities of chronic nicotine use have been associated with numerous negative consequences to human health, one possible benefit of nicotine exposure has been uncovered. The discovery of an inverse correlation between smoking and Parkinson’s disease, and later Alzheimer’s disease as well, motivated investigation of nicotine as a neuroprotective agent. Some studies have demonstrated that nicotine elicits improvements in cognitive function. The hippocampus, along with the subventricular zone (SVZ), is a distinct brain region that allow for ongoing postnatal neurogenesis throughout adulthood and plays a major role in certain cognitive behaviors like learning and memory. Therefore, one hypothesis underlying nicotine-induced neuroprotection is possible effects on neural stem cells and neural precursor cells. On the other hand, nicotine withdrawal frequently leads to cognitive impairments, particularly in hippocampal-dependent behaviors, possibly suggesting an impairment of hippocampal neurogenesis with nicotine exposure. This review discusses the current body of evidence on nicotine’s effects on neural stem cells and neural progenitors. Changes in neural stem cell proliferation, survival, intracellular dynamics, and differentiation following acute and chronic nicotine exposure are examined.

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Molecular Genetic Analysis of Neural Stem Cells After Space Flight And Simulated Microgravity on Earth

Biotechnology and Bioengineering ◽

10.1002/bit.27858 ◽

2021 ◽

Author(s):

Yilin Han ◽

Lukas Zeger ◽

Rekha Tripathi ◽

Marcel Egli ◽

Fabian Ille ◽

...

Keyword(s):

Stem Cells ◽

Genetic Analysis ◽

Neural Stem Cells ◽

Space Flight ◽

Simulated Microgravity ◽

Molecular Genetic ◽

Molecular Genetic Analysis

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Ghrelin gene products rescue cultured adult rat hippocampal neural stem cells from high glucose insult

Journal of Molecular Endocrinology ◽

10.1530/jme-16-0096 ◽

2016 ◽

Vol 57 (3) ◽

pp. 171-184 ◽

Cited By ~ 3

Author(s):

Sehee Kim ◽

Chanyang Kim ◽

Seungjoon Park

Keyword(s):

Stem Cells ◽

Neural Stem Cells ◽

High Glucose ◽

Hippocampal Neurogenesis ◽

Adult Hippocampal Neurogenesis ◽

Gene Products ◽

Growth Hormone Secretagogue ◽

Phosphohistone H3 ◽

Ghrelin Gene ◽

Hippocampal Neural Stem Cells

Adult hippocampal neurogenesis is decreased in type 2 diabetes, and this impairment appears to be important in cognitive dysfunction. Previous studies suggest that ghrelin gene products (acylated ghrelin (AG), unacylated ghrelin (UAG) and obestatin (OB)) promote neurogenesis. Therefore, we hypothesize that ghrelin gene products may reduce the harmful effects of high glucose (HG) on hippocampal neural stem cells (NSCs). The aim of this study was to investigate the role of these peptides on the survival of cultured hippocampal NSCs exposed to HG insult. Treatment of hippocampal NSCs with AG, UAG or OB inhibited HG-induced cell death and apoptosis. Exposure of cells to the growth hormone secretagogue receptor 1a antagonist abolished the protective effects of AG against HG toxicity, whereas those of UAG or OB were preserved. All three peptides attenuated HG-induced decrease in BrdU-labeled and phosphohistone-H3-labeled cells. We also investigated the effects of ghrelin gene products on the regulation of apoptosis at the mitochondrial level. AG, UAG or OB rescued hippocampal NSCs from HG insult by inhibiting intracellular and mitochondrial reactive oxygen species generation and stabilizing mitochondrial transmembrane potential. In addition, cells treated with ghrelin gene products showed an increased Bcl-2 and decreased Bax levels, thereby increasing the Bcl-2/Bax ratio, inhibiting cytochrome c release and preventing caspase-3 activation. Finally, AG-, UAG- or OB-mediated protection was dependent on the activities of adenosine monophosphate-activated protein kinase/uncoupling protein 2 pathway. Our data indicate that ghrelin gene products may act as survival factors that preserve mitochondrial function and inhibit oxidative stress-induced apoptosis.

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