[P109]: Neural progenitor cells are impaired in extremely preterm infants with ischemic brain injuries

2006 ◽  
Vol 24 (8) ◽  
pp. 542-542
Author(s):  
K. Deguchi ◽  
S. Takashima ◽  
D. Armstrong ◽  
K. Inoue
Keyword(s):  
Progenitor Cells ◽  
Preterm Infants ◽  
Neural Progenitor Cells ◽  
Brain Injuries ◽  
Neural Progenitor ◽  
Ischemic Brain ◽  
Extremely Preterm ◽  
Extremely Preterm Infants

scholarly journals TNF-α Pretreatment Improves the Survival and Function of Transplanted Human Neural Progenitor Cells Following Hypoxic-Ischemic Brain Injury

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1195
Author(s):  
Miri Kim ◽  
Kwangsoo Jung ◽  
Younhee Ko ◽  
Il-Sun Kim ◽  
Kyujin Hwang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Infarct Volume ◽  
Fetal Brain ◽  
Neural Progenitor ◽  
Great Promise ◽  
Therapeutic Effects ◽  
Ischemic Brain ◽  
Tnf Α

Neural progenitor cells (NPCs) therapy offers great promise in hypoxic-ischemic (HI) brain injury. However, the poor survival of implanted NPCs in the HI host environment limits their therapeutic effects. Tumor necrosis factor-alpha (TNF-α) is a pleiotropic cytokine that is induced in response to a variety of pathological processes including inflammation and immunity. On the other hand, TNF-α has protective effects on cell apoptosis and death and affects the differentiation, proliferation, and survival of neural stem/progenitor cells in the brain. The present study investigated whether TNF-α pretreatment on human NPCs (hNPCs) enhances the effectiveness of cell transplantation therapy under ischemic brain. Fetal brain tissue-derived hNPCs were pretreated with TNF-α before being used in vitro experiments or transplantation. TNF-α significantly increased expression of cIAP2, and the use of short hairpin RNA-mediated knockdown of cIAP2 demonstrated that cIAP2 protected hNPCs against HI-induced cytotoxicity. In addition, pretreatment of hNPCs with TNF-α mediated neuroprotection by altering microglia polarization via increased expression of CX3CL1 and by enhancing expression of neurotrophic factors. Furthermore, transplantation of TNF-α-treated hNPCs reduced infarct volume and improved neurological functions in comparison with non-pretreated hNPCs or vehicle. These findings show that TNF-α pretreatment, which protects hNPCs from HI-injured brain-induced apoptosis and increases neuroprotection, is a simple and safe approach to improve the survival of transplanted hNPCs and the therapeutic efficacy of hNPCs in HI brain injury.

Survival and differentiation of neural progenitor cells derived from embryonic stem cells and transplanted into ischemic brain

2005 ◽  
Vol 103 (2) ◽  
pp. 304-310 ◽  
Author(s):  
Yasushi Takagi ◽  
Masaki Nishimura ◽  
Asuka Morizane ◽  
Jun Takahashi ◽  
Kazuhiko Nozaki ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Fluorescent Protein ◽  
Embryonic Stem ◽  
Neural Progenitor ◽  
Ischemic Brain ◽  
Content Type ◽  
Fine Print

Object. Cell replacement therapy including the use of embryonic stem cells (ESCs) may represent a novel treatment for damage from stroke. In this study, the authors transplanted neural progenitor cells (NPCs) derived from ESCs into ischemic brain and analyzed their survival and differentiation. Methods. Multipotential NPCs were generated from ESCs by using the stromal cell—derived inducing activity method. These cells could differentiate in vitro into neurons, glia, and oligodendrocytes, thus revealing them to be neural stem cells. The NPCs were then transplanted into ischemic brain. At 2 weeks postischemia, the transplanted cells occupied 18.8 ± 2.5% of the hemispheric area; by 4 weeks postischemia, 26.5 ± 4% of the hemisphere. At 4 weeks after transplantation, green fluorescent protein (GFP)—positive transplanted cells showed mature neuronal morphological features. The authors also investigated the expression of differentiation markers and various neurotransmitters. Transplanted cells were immunopositive for neuronal nuclei, β-tubulin-III, and glial fibrillary acidic protein. Of the GFP-positive cells, 33.3 ± 11.5% were positive for glutamate decarboxylase, 13.3 ± 5.8% for glutamate, 2.1 ± 2.5% for tyrosine hydroxylase, 1.8 ± 2% for serotonin, and 0.4 ± 0.2% for choline acetyltransferase. Conclusions. The authors confirmed the survival and differentiation of ESC-derived NPCs transplanted into the ischemic brain. Surviving transplanted cells expressed several neural markers and neurotransmitters. These findings indicate that these cells can function in the brain.

Abstract 2976: Sildenafil Enhances Neurogenesis And Oligodendrogenesis In The Ischemic Brain Of Aged Mouse

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Rui Lan Zhang ◽  
Michael Chopp ◽  
Cynthia Roberts ◽  
Min Wei ◽  
Xinli Wang ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Pde5 Inhibitor ◽  
Neural Progenitor ◽  
Artery Occlusion ◽  
Immunofluorescent Staining ◽  
Aged Mouse ◽  
Ischemic Brain ◽  
Physics Department

Sildenafil enhances neurogenesis and oligodendrogenesis in the ischemic brain of aged mouse Rui Lan Zhang 1 , Michael Chopp 1,2 Cynthia Roberts 1 , Min Wei 1 , Xinli Wang 1 , Xianshuang Liu 1 , Zheng Gang Zhang 1 Departments of 1 Neurology and Henry Ford Hospital, Detroit, MI, USA 2 Oakland University, Physics Department, Rochester, MI, USA. Background and Purpose: Nestin lineage neural progenitor cells contribute to neurogenesis in adult rodent brain under non-ischemic and ischemic conditions. The present study investigated the effect of sildenafil, a potent phosphodiesterase 5 (PDE5) inhibitor, on nestin lineage neural progenitor cells in the aged mouse after stroke. Methods: Male Nestin-CreER T2 ;R26R-stop-YFP mice at age 16 months were used. Tamoxifen was daily injected for 5 days to activate Cre/loxP system under control of the nestin promoter, leading to permanent YFP labeling of nestin lineage cells. These mice were subjected to permanent middle cerebral artery occlusion (MCAo) 14 days after the last tamoxifen injection. Sildenafil at 10mg/kg (n=11) or saline (n=10) was aadministered daily for 7 days starting 1 day after MCAo. All mice were sacrificed 30 days after MCAo. The number of nestin lineage cells and their fate were analyzed using immunohistochemistry staining. Results: Double immunofluorescent staining confirmed YFP positive cells were nestin positive. Unbiased stereological analysis revealed that sildenafil treatment significantly increased (p<0.05) the number of nestin linage cells in the ischemic subventricular zone (SVZ, 803 ± 28 vs 657 ± 41 in saline), striatum (3739 ± 162 vs 3029 ± 144 in saline), and corpus callosum (2957 ± 86 vs 2578 ± 117 in saline). Phenotype analysis showed that sildenafil substantially augmented the number of nestin lineage neuroblasts identified by doublecortin positive cells (19.4 ± 1.6 % vs 12.9 ± 1.1 % in saline), nestin lineage mature neurons measured by NeuN (6.2 ± 0.8 % vs 3.0 ± 0.6 %) and calbindin (10.8 ± 0.9 vs 7.2 ± 1.1) positive cells in the ischemic striatum. Sildenafil also significantly (p<0.05) increased the number of nestin lineage oligodendrocytes measured by 2’, 3’-cyclic nucleotide, 3’-phosphodiesterase (CNPase) positive cells in ischemic striatum (21.3 ± 1.2 vs 19.9 ± 1.4 in saline) and corpus callosum (18.9 ± 1.4 vs 14.4 ± 1.3 in saline). Conclusion: Our data demonstrate that sildenafil enhances neurogenesis and oligodendrogenesis in the ischemic brain of the aged mouse, which could contribute sildenafil-improved neurological outcome after stroke which we have demonstrated.

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