scholarly journals Proliferation and Glia-Directed Differentiation of Neural Stem Cells in the Subventricular Zone of the Lateral Ventricle and the Migratory Pathway to the Lesions after Cortical Devascularization of Adult Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Feng Wan ◽  
Hua-Jing Bai ◽  
Jun-Qi Liu ◽  
Mo Tian ◽  
Yong-Xue Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Corpus Callosum ◽  
Subventricular Zone ◽  
Lateral Ventricle ◽  
Control Group ◽  
Directed Differentiation ◽  
Cortical Lesions ◽  
Adult Rats ◽  
And Migration ◽  
Migratory Pathway

We investigated the effects of cortical devascularization on the proliferation, differentiation, and migration of neural stem cells (NSCs) in the subventricular zone (SVZ) of the lateral ventricle of adult rats. 60 adult male Wistar rats were randomly divided into control group and devascularized group. At 15 and 30 days after cerebral cortices were devascularized, rats were euthanized and immunohistochemical analysis was performed. The number of PCNA-, Vimentin-, and GFAP-positive cells in the bilateral SVZ of the lateral wall and the superior wall of the lateral ventricles of 15- and 30-day devascularized groups increased significantly compared with the control group (P<0.05andP<0.01). The area density of PCNA-, Vimentin-, and GFAP-positive cells in cortical lesions of 15- and 30-day devascularized groups increased significantly compared with the control group (P<0.05andP<0.01). PCNA-, GFAP-, and Vimentin-positive cells in the SVZ migrated through the rostral migratory stream (RMS), and PCNA-, GFAP-, and Vimentin-positive cells from both the ipsilateral and contralateral dorsolateral SVZ (dl-SVZ) migrated into the corpus callosum (CC) and accumulated, forming a migratory pathway within the CC to the lesioned site. Our study suggested that cortical devascularization induced proliferation, glia-directed differentiation, and migration of NSCs from the SVZ through the RMS or directly to the corpus callosum and finally migrating radially to cortical lesions. This may play a significant role in neural repair.

scholarly journals Neuroprotective effects of dexmedetomidine on the ketamine-induced disruption of the proliferation and differentiation of developing neural stem cells in the subventricular zone

2020 ◽  
Author(s):  
Huanhuan Sha ◽  
Peipei Peng ◽  
Bing Li ◽  
Guohua Wei ◽  
Juan Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Subventricular Zone ◽  
Pediatric Anesthesia ◽  
Brdu Incorporation ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Proliferation And Differentiation ◽  
Ketamine Anesthesia ◽  
Β Tubulin

Abstract Background: Recently, the number of neonatal patients receiving surgery under general anesthesia has increased. Ketamine disrupts the proliferation and differentiation of developing neural stem cells (NSCs). Therefore, the safe use of ketamine in pediatric anesthesia has been an issue of increasing concern among anesthesiologists and the children’s parents. Dexmedetomidine (DEX) is widely used in sedation, as an antianxiety agent and for analgesia. DEX has recently been shown to provide neuroprotection against anesthetic-induced neurotoxicity in the developing brain. The aim of this in vivo study was to investigate whether DEX exerted neuroprotective effects on the proliferation and differentiation of NSCs in the subventricular zone (SVZ) following neonatal ketamine exposure. Methods: Postnatal day 7 (PND-7) male Sprague-Dawley rats were equally divided into the following 5 groups: Control group (n=8), Ketamine group (n=8), 1 μg/kg DEX+Ketamine group (n=8), 5 μg/kg DEX+Ketamine group (n=8) and 10 μg/kg DEX+Ketamine group (n=8). The proliferation and differentiation of NSCs in the SVZ were assessed using immunostaining with BrdU incorporation. The levels of Nestin and β-tubulin III in the SVZ were measured using Western blot analyses. Apoptosis was assessed by detecting the levels of the cleaved caspase-3 protein using Western blotting. Results: Neonatal ketamine exposure significantly inhibited NSC proliferation and astrocytic differentiation in the SVZ, and neuronal differentiation was markedly increased. Furthermore, pretreatment with moderate (5 μg/kg) or high doses (10 μg/kg) of DEX reversed the ketamine-induced disturbances in the proliferation and differentiation of NSCs. Meanwhile, neonatal ketamine exposure significantly decreased the expression of Nestin and increased the expression of β-tubulin III in the SVZ compared with the Control group. Treatment with 10 μg/kg DEX notably reversed the ketamine-induced changes in the levels of Nestin and β-tubulin III. In addition, a pretreatment with 10 μg/kg DEX before ketamine anesthesia prevented apoptosis in the SVZ induced by neonatal ketamine exposure. Conclusions: Based on our findings, DEX may exert neuroprotective effects on the proliferation and differentiation of NSCs in the SVZ of neonatal rats in a repeated ketamine anesthesia model.

scholarly journals Neural Stem Cells of the Subventricular Zone Contribute to Neuroprotection of the Corpus Callosum after Cuprizone-Induced Demyelination

2019 ◽  
Vol 39 (28) ◽  
pp. 5481-5492 ◽  
Author(s):  
Erica Butti ◽  
Marco Bacigaluppi ◽  
Linda Chaabane ◽  
Francesca Ruffini ◽  
Elena Brambilla ◽  
...  
Keyword(s):  
Stem Cells ◽  
Corpus Callosum ◽  
Neural Stem Cells ◽  
Subventricular Zone

scholarly journals Troxerutin flavonoid has neuroprotective properties and increases neurite outgrowth and migration of neural stem cells from the subventricular zone

PLoS ONE ◽  
2020 ◽  
Vol 15 (8) ◽  
pp. e0237025
Author(s):  
Muhammad Irfan Masood ◽  
Karl Herbert Schäfer ◽  
Mahrukh Naseem ◽  
Maximilian Weyland ◽  
Peter Meiser
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neurite Outgrowth ◽  
Subventricular Zone ◽  
And Migration

MicroRNA (miR)-29 Modified Bone Marrow Stem Cells (BMSCs) Regulating Wnt-β-Catenin-p53 Pathway to Inhibit the Migration and Proliferation of Conjunctival Fibroblasts

2021 ◽  
Vol 11 (8) ◽  
pp. 1517-1523
Author(s):  
Shibo Xiong ◽  
Pengcheng Huang ◽  
Sumin Xu ◽  
Aimin Li
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
P53 Protein ◽  
Fibroblast Cell ◽  
Scratch Test ◽  
Bone Marrow Stem Cells ◽  
Control Group ◽  
P53 Pathway ◽  
Protein Expressions ◽  
And Migration

To explore the mechanism of miR-29 modified bone marrow stem cells (BMSCs) in regulating the Wnt/β-Catenin-p53 pathway to inhibit the migration and proliferation of conjunctival fibroblasts. New Zealand rabbit BMSCs were randomly divided into control group, miR-29NC group, and miR-29mimic group. MTT assay, cell scratch test, and Western blot were used to detect the proliferation, migration, and protein expressions in constituent fibroblast. Cell proliferation in the miR-29mimic group was attenuated at 24 h and 48 h (P <0.05). The expression of miR-29 in miR-29 mimic group was upregulated, while Wnt/β-Catenin-p53 protein was decreased (P < 0.05). MiR-29 modified BMSC can inhibit the expression of Wnt/β-Catenin-p53 pathway and suppress the proliferation and migration of conjunctival fibroblasts.

scholarly journals Activated Neural Stem Cells Contribute to Stroke-Induced Neurogenesis and Neuroblast Migration toward the Infarct Boundary in Adult Rats

2004 ◽  
Vol 24 (4) ◽  
pp. 441-448 ◽  
Author(s):  
Ruilan Zhang ◽  
Zhenggang Zhang ◽  
Lei Wang ◽  
Ying Wang ◽  
Anton Gousev ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Subventricular Zone ◽  
Proliferating Cells ◽  
Adult Rats ◽  
Antimitotic Agent ◽  
Neuroblast Migration ◽  
Ipsilateral Striatum

Stroke increases neurogenesis. The authors investigated whether neural stem cells or progenitor cells in the adult subventricular zone (SVZ) of rats contribute to stroke-induced increase in neurogenesis. After induction of stroke in rats, the numbers of cells immunoreactive to doublecortin, a marker for immature neurons, increased in the ipsilateral SVZ and striatum. Infusion of an antimitotic agent (cytosine-β-D-arabiofuranoside, Ara-C) onto the ipsilateral cortex eliminated more than 98% of actively proliferating cells in the SVZ and doublecortin-positive cells in the ipsilateral striatum. However, doublecortin-positive cells rapidly replenished after antimitotic agent depletion of actively proliferating cells. Depleting the numbers of actively proliferating cells in vivo had no effect on the numbers of neurospheres formed in vitro, yet the numbers of neurospheres derived from stroke rats significantly ( P < 0.05) increased. Neurospheres derived from stroke rats self-renewed and differentiated into neurons and glia. In addition, doublecortin-positive cells generated in the SVZ migrated in a chainlike structure toward ischemic striatum. These findings indicate that in the adult stroke brain, increases in recruitment of neural stem cells contribute to stroke-induced neurogenesis, and that newly generated neurons migrate from the SVZ to the ischemic striatum.

scholarly journals Neuroprotective effects of dexmedetomidine on the ketamine-induced disruption of the proliferation and differentiation of developing neural stem cells in the subventricular zone

2020 ◽  
Author(s):  
Huanhuan Sha ◽  
Peipei Peng ◽  
Bing Li ◽  
Guohua Wei ◽  
Juan Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Subventricular Zone ◽  
Pediatric Anesthesia ◽  
Brdu Incorporation ◽  
Control Group ◽  
Neuroprotective Effects ◽  
Proliferation And Differentiation ◽  
Ketamine Anesthesia ◽  
Β Tubulin

Abstract Background: Recently, the number of neonatal patients receiving surgery under general anesthesia has increased. Ketamine disrupts the proliferation and differentiation of developing neural stem cells (NSCs). Therefore, the safe use of ketamine in pediatric anesthesia has been an issue of increasing concern among anesthesiologists and the children’s parents. Dexmedetomidine (DEX) is widely used in sedation, as an antianxiety agent and for analgesia. DEX has recently been shown to provide neuroprotection against anesthetic-induced neurotoxicity in the developing brain. The aim of this in vivo study was to investigate whether DEX exerted neuroprotective effects on the proliferation and differentiation of NSCs in the subventricular zone (SVZ) following neonatal ketamine exposure.Methods: Postnatal day 7 (PND-7) male Sprague-Dawley rats were equally divided into the following 5 groups: Control group (n=8), Ketamine group (n=8), 1 μg/kg DEX+Ketamine group (n=8), 5 μg/kg DEX+Ketamine group (n=8) and 10 μg/kg DEX+Ketamine group (n=8). The proliferation and differentiation of NSCs in the SVZ were assessed using immunostaining with BrdU incorporation. The levels of Nestin and β-tubulin III in the SVZ were measured using Western blot analyses. Apoptosis was assessed by detecting the levels of the cleaved caspase-3 protein using Western blotting.Results: Neonatal ketamine exposure significantly inhibited NSC proliferation and astrocytic differentiation in the SVZ, and neuronal differentiation was markedly increased. Furthermore, pretreatment with moderate (5 μg/kg) or high doses (10 μg/kg) of DEX reversed the ketamine-induced disturbances in the proliferation and differentiation of NSCs. Meanwhile, neonatal ketamine exposure significantly decreased the expression of Nestin and increased the expression of β-tubulin III in the SVZ compared with the Control group. Treatment with 10 μg/kg DEX notably reversed the ketamine-induced changes in the levels of Nestin and β-tubulin III. In addition, a pretreatment with 10 μg/kg DEX before ketamine anesthesia prevented apoptosis in the SVZ induced by neonatal ketamine exposure.Conclusions: Based on our findings, DEX may exert neuroprotective effects on the proliferation and differentiation of NSCs in the SVZ of neonatal rats in a repeated ketamine anesthesia model.

scholarly journals Modulation of LXR signaling altered the dynamic activity of human colon adenocarcinoma cancer stem cells in vitro

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hassan Dianat-Moghadam ◽  
Mostafa Khalili ◽  
Mohsen Keshavarz ◽  
Mehdi Azizi ◽  
Hamed Hamishehkar ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Abc Transporters ◽  
Flow Cytometric Analysis ◽  
Metabolic Enzymes ◽  
Colorectal Cancers ◽  
Control Group ◽  
Dependent Manner ◽  
Protein Levels ◽  
And Migration

Abstract Background The expansion and metastasis of colorectal cancers are closely associated with the dynamic growth of cancer stem cells (CSCs). This study aimed to explore the possible effect of LXR (a regulator of glycolysis and lipid hemostasis) in the tumorgenicity of human colorectal CD133 cells. Methods Human HT-29 CD133+ cells were enriched by MACS and incubated with LXR agonist (T0901317) and antagonist (SR9243) for 72 h. Cell survival was evaluated using MTT assay and flow cytometric analysis of Annexin-V. The proliferation rate was measured by monitoring Ki-67 positive cells using IF imaging. The modulation of LXR was studied by monitoring the activity of all factors related to ABC transporters using real-time PCR assay and western blotting. Protein levels of metabolic enzymes such as PFKFB3, GSK3β, FASN, and SCD were also investigated upon treatment of CSCs with LXR modulators. The migration of CSCs was monitored after being exposed to LXR agonist using scratch and Transwell insert assays. The efflux capacity was measured using hypo-osmotic conditions. The intracellular content of reactive oxygen species was studied by DCFH-DA staining. Results Data showed incubation of CSCs with T0901317 and SR9243 reduced the viability of CD133 cells in a dose-dependent manner compared to the control group. The activation of LXR up-regulated the expression and protein levels of ABC transporters (ABCA1, ABCG5, and ABCG8) compared to the non-treated cells (p < 0.05). Despite these effects, LXR activation suppressed the proliferation, clonogenicity, and migration of CD133 cells, and increased hypo-osmotic fragility (p < 0.05). We also showed that SR9243 inhibited the proliferation and clonogenicity of CD133 cells through down-regulating metabolic enzymes PFKFB3, GSK3β, FASN, and SCD as compared with the control cells (p < 0.05). Intracellular ROS levels were increased after the inhibition of LXR by SR9243 (p < 0.05). Calling attention, both T0901317 and SR9243 compounds induced apoptotic changes in cancer stem cells (p < 0.05). Conclusions The regulation of LXR activity can be considered as a selective targeting of survival, metabolism, and migration in CSCs to control the tumorigenesis and metastasis in patients with advanced colorectal cancers.

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