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

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.

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

2016 ◽  
Vol 57 (3) ◽  
pp. 171-184 ◽  
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.

scholarly journals Ablation of the microRNA‐17‐92 cluster in neural stem cells diminishes adult hippocampal neurogenesis and cognitive function

2019 ◽  
Vol 33 (4) ◽  
pp. 5257-5267 ◽  
Author(s):  
Wan Long Pan ◽  
Michael Chopp ◽  
Baoyan Fan ◽  
Ruilan Zhang ◽  
Xinli Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cognitive Function ◽  
Neural Stem Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis

scholarly journals Autophagic death of neural stem cells mediates chronic stress-induced decline of adult hippocampal neurogenesis and cognitive deficits

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S487
Author(s):  
Seonghee Jung ◽  
Seongwon Choe ◽  
Hanwoong Woo ◽  
Hyeonjeong Jeong ◽  
Hyun-Kyu An ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Chronic Stress ◽  
Cognitive Deficits ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis

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

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Tian Lin ◽  
Juan Du ◽  
Li Liu ◽  
Zheng Wu ◽  
Xiangkai Kong ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Simulated Microgravity ◽  
Hippocampal Neurogenesis ◽  
Microglia Activation ◽  
Tail Suspension ◽  
Key Factors ◽  
Adult Rats ◽  
Chip Analysis ◽  
Proinflammatory Factors

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.

scholarly journals Circadian and ultradian glucocorticoid rhythmicity: Implications for the effects of glucocorticoids on neural stem cells and adult hippocampal neurogenesis

2016 ◽  
Vol 41 ◽  
pp. 44-58 ◽  
Author(s):  
Carlos P. Fitzsimons ◽  
Joe Herbert ◽  
Marijn Schouten ◽  
Onno C. Meijer ◽  
Paul J. Lucassen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis

scholarly journals Activation of neural stem cells from quiescence drives reactive hippocampal neurogenesis after alcohol dependence

2018 ◽  
Vol 133 ◽  
pp. 276-288 ◽  
Author(s):  
Dayna M. Hayes ◽  
Chelsea G. Nickell ◽  
Kevin Y. Chen ◽  
Justin A. McClain ◽  
Megan M. Heath ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Alcohol Dependence ◽  
Hippocampal Neurogenesis

scholarly journals Active Fraction Combination From Liuwei Dihuang Decoction Improves Adult Hippocampal Neurogenesis and Neurogenic Microenvironment in Cranially Irradiated Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Mingxiao Wei ◽  
Shufang Feng ◽  
Lin Zhang ◽  
Chen Wang ◽  
Shasha Chu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Dorsal Hippocampus ◽  
Cranial Irradiation ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Active Fraction ◽  
Cranial Radiotherapy ◽  
Contextual Fear ◽  
Immature Neurons

Background: Cranial radiotherapy is clinically used in the treatment of brain tumours; however, the consequent cognitive and emotional dysfunctions seriously impair the life quality of patients. LW-AFC, an active fraction combination extracted from classical traditional Chinese medicine prescription Liuwei Dihuang decoction, can improve cognitive and emotional dysfunctions in many animal models; however, the protective effect of LW-AFC on cranial irradiation–induced cognitive and emotional dysfunctions has not been reported. Recent studies indicate that impairment of adult hippocampal neurogenesis (AHN) and alterations of the neurogenic microenvironment in the hippocampus constitute critical factors in cognitive and emotional dysfunctions following cranial irradiation. Here, our research further investigated the potential protective effects and mechanisms of LW-AFC on cranial irradiation–induced cognitive and emotional dysfunctions in mice.Methods: LW-AFC (1.6 g/kg) was intragastrically administered to mice for 14 days before cranial irradiation (7 Gy γ-ray). AHN was examined by quantifying the number of proliferative neural stem cells and immature neurons in the dorsal and ventral hippocampus. The contextual fear conditioning test, open field test, and tail suspension test were used to assess cognitive and emotional functions in mice. To detect the change of the neurogenic microenvironment, colorimetry and multiplex bead analysis were performed to measure the level of oxidative stress, neurotrophic and growth factors, and inflammation in the hippocampus.Results: LW-AFC exerted beneficial effects on the contextual fear memory, anxiety behaviour, and depression behaviour in irradiated mice. Moreover, LW-AFC increased the number of proliferative neural stem cells and immature neurons in the dorsal hippocampus, displaying a regional specificity of neurogenic response. For the neurogenic microenvironment, LW-AFC significantly increased the contents of superoxide dismutase, glutathione peroxidase, glutathione, and catalase and decreased the content of malondialdehyde in the hippocampus of irradiated mice, accompanied by the increase in brain-derived neurotrophic factor, insulin-like growth factor-1, and interleukin-4 content. Together, LW-AFC improved cognitive and emotional dysfunctions, promoted AHN preferentially in the dorsal hippocampus, and ameliorated disturbance in the neurogenic microenvironment in irradiated mice.Conclusion: LW-AFC ameliorates cranial irradiation–induced cognitive and emotional dysfunctions, and the underlying mechanisms are mediated by promoting AHN in the dorsal hippocampus and improving the neurogenic microenvironment. LW-AFC might be a promising therapeutic agent to treat cognitive and emotional dysfunctions in patients receiving cranial radiotherapy.

scholarly journals IL-1β and HMGB1 are anti-neurogenic to endogenous neural stem cells in the sclerotic epileptic human hippocampus

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Malik Zaben ◽  
Niels Haan ◽  
Feras Sharouf ◽  
Aminul Ahmed ◽  
Lars E. Sundstrom ◽  
...  
Keyword(s):  
Stem Cells ◽  
Animal Models ◽  
Neural Stem Cells ◽  
Temporal Lobe Epilepsy ◽  
Learning And Memory ◽  
Temporal Lobe ◽  
Hippocampal Neurogenesis ◽  
Human Hippocampus ◽  
Dependent Learning ◽  
Endogenous Neural Stem Cells

Abstract Background The dentate gyrus exhibits life-long neurogenesis of granule-cell neurons, supporting hippocampal dependent learning and memory. Both temporal lobe epilepsy patients and animal models frequently have hippocampal-dependent learning and memory difficulties and show evidence of reduced neurogenesis. Animal and human temporal lobe epilepsy studies have also shown strong innate immune system activation, which in animal models reduces hippocampal neurogenesis. We sought to determine if and how neuroinflammation signals reduced neurogenesis in the epileptic human hippocampus and its potential reversibility. Methods We isolated endogenous neural stem cells from surgically resected hippocampal tissue in 15 patients with unilateral hippocampal sclerosis. We examined resultant neurogenesis after growing them either as neurospheres in an ideal environment, in 3D cultures which preserved the inflammatory microenvironment and/or in 2D cultures which mimicked it. Results 3D human hippocampal cultures largely replicated the cellular composition and inflammatory environment of the epileptic hippocampus. The microenvironment of sclerotic human epileptic hippocampal tissue is strongly anti-neurogenic, with sustained release of the proinflammatory proteins HMGB1 and IL-1β. IL-1β and HMGB1 significantly reduce human hippocampal neurogenesis and blockade of their IL-1R and TLR 2/4 receptors by IL1Ra and Box-A respectively, significantly restores neurogenesis in 2D and 3D culture. Conclusion Our results demonstrate a HMGB1 and IL-1β-mediated environmental anti-neurogenic effect in human TLE, identifying both the IL-1R and TLR 2/4 receptors as potential drug targets for restoring human hippocampal neurogenesis in temporal lobe epilepsy.

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