Only in Titles

           Search results for: Human Glial Derived Neurotrophic Factor GDNF   

paperclip

#29656478   // Save this To Up

Transplantation of Neural Progenitor Cells Expressing Glial Cell Line-Derived Neurotrophic Factor into the Motor Cortex as a Strategy to Treat Amyotrophic Lateral Sclerosis.

Early dysfunction of cortical motor neurons may underlie the initiation of amyotrophic lateral sclerosis (ALS). As such, the cortex represents a critical area of ALS research and a promising therapeutic target. In the current study, human cortical-derived neural progenitor cells engineered to secrete glial cell line-derived neurotrophic factor (GDNF) were transplanted into the SOD1 ALS rat cortex, where they migrated, matured into astrocytes, and released GDNF. This protected motor neurons, delayed disease pathology and extended survival of the animals. These same cells injected into the cortex of cynomolgus macaques survived and showed robust GDNF expression without adverse effects. Together this data suggests that introducing cortical astrocytes releasing GDNF represents a novel promising approach to treating ALS. Stem Cells 2018.

1055 related Products with: Transplantation of Neural Progenitor Cells Expressing Glial Cell Line-Derived Neurotrophic Factor into the Motor Cortex as a Strategy to Treat Amyotrophic Lateral Sclerosis.

Epidermal Growth Factor ( Epidermal Growth Factor ( Human Glial Derived Neuro Human Stromal Cell-Derive Mouse Stromal Cell-Derive glial cells missing homol Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri thymic dendritic cell-der GLP 1 ELISA Kit, Rat Gluc CometAssay Control Cells Neutral CometAssay Contro

Related Pathways

paperclip

#29649411   // Save this To Up

The In Vitro Differentiation of GDNF Gene-Engineered Amniotic Fluid-Derived Stem Cells into Renal Tubular Epithelial-Like Cells.

Amniotic fluid is an alternative source of stem cells, and human amniotic fluid-derived stem cells (AFSCs) obtained from a small amount of amniotic fluid collected during the second trimester represent a novel source for use in regenerative medicine. These AFSCs are characterized by lower diversity, a higher proliferation rate, and a wider differentiation capability than adult mesenchymal stem cells. AFSCs are selected based on the cell surface marker c-kit receptor (CD117) using immunomagnetic sorting. Glial cell line-derived neurotrophic factor (GDNF) is expressed during early kidney development and regulates the proliferation and differentiation of stem cells in vitro. In this study, c-kit-sorted AFSCs were induced toward osteogenic or adipogenic differentiation. AFSCs engineered via the insertion of GDNF were cocultured with mouse renal tubular epithelial cells (mRTECs), which were preconditioned by hypoxia-reoxygenation in vitro. After coculture for 8 days, AFSCs differentiation into epithelial-like cells was evaluated by performing immunofluorescence, flow cytometry, and quantitative real-time polymerase chain reaction to identify cells expressing the renal epithelial markers, cytokeratin 18 (CK18), E-cadherin, aquaporin-1 (AQP1), and paired box 2 gene (Pax2). The GDNF gene enhanced AFSCs differentiation into RTECs. AFSCs possess self-renewal ability and multiple differentiation potential and thus represent a new source of stem cells.

2081 related Products with: The In Vitro Differentiation of GDNF Gene-Engineered Amniotic Fluid-Derived Stem Cells into Renal Tubular Epithelial-Like Cells.

Macrophage Colony Stimula Macrophage Colony Stimula anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Epidermal Growth Factor ( Epidermal Growth Factor ( GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi

Related Pathways

paperclip

#29634418   // Save this To Up

Demethylation of GFRA4 Promotes Cell Proliferation and Invasion in Hirschsprung Disease.

Hirschsprung disease (HSCR) is congenital intestinal aganglionosis attributed to a failure to migrate and survive of neural crest-derived cells. Glial cell-derived neurotrophic factor alpha 4 (GFRA4) is expressed in the derivatives of the neural crest in the enteric nervous system, but whether it is related with HSCR still remains unclear. This study was designed to investigate its role and epigenetic mechanisms in HSCR in vitro. The expression of GFRA4 mRNA in HSCR tissues was determined using quantitative real-time PCR analysis. In this study, we found that GFRA4 expression was significantly reduced in HSCR tissues and cells through GFRA4 methylation by quantitative real-time PCR analysis, methylation-specific PCR, and bisulfite sequencing PCR. DNA methyltransferase inhibitor, 5-AzaC, concomitantly upregulated the protein levels of GFRA4, as well as DNA methyltransferase1 (DNMT1) and DNMT2 in SH-5YSY cells. Moreover, we found upregulated GFRA4 significantly promoted cell proliferation, cell cycle progression and invasion, but inhibited apoptosis in SH-5YSY cells, whereas GFRA4 knockdown caused the opposite effects in SH-5YSY cells by CCK-8, 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and Transwell assays. In conclusion, our results support that aberrant CpG hypermethylation at least partly accounts for GFRA4 silencing in HSCR, which impairs its protective role in enteric nervous system.

2890 related Products with: Demethylation of GFRA4 Promotes Cell Proliferation and Invasion in Hirschsprung Disease.

Cultrex 24 Well BME Cell Cultrex 24 Well Laminin I Cultrex 96 Well Laminin I Cultrex 24 Well Collagen Cultrex 96 Well Collagen Cultrex 24 Well Collagen Cultrex 96 Well Collagen Cultrex In Vitro Angiogen Cultrex96 Well 3D BME Cel Alamar Blue™, REDOX ind Alamar Blue™, REDOX ind anti HSV (II) gB IgG1 (mo

Related Pathways

  •  
  • No related Items
paperclip

#29562865   // Save this To Up

Regulatable Lentiviral Hematopoietic Stem Cell Gene Therapy in a Mouse Model of Parkinson's Disease.

Glial cell line-derived neurotrophic factor (GDNF) exhibits potent neuroprotective properties in preclinical models of Parkinson's disease (PD), but challenges in GDNF delivery have been reported from clinical trials. To address this barrier, we developed a hematopoietic stem cell transplantation-based macrophage-mediated GDNF therapy platform. Here, we introduced a regulatable lentiviral vector (LV-MSP-Tet-Off-hGDNF) to allow the expression of human GDNF (hGDNF) to be adjusted or stopped by oral administration of doxycycline (Dox). C57BL/6J mice were lethally irradiated with head protection and then transplanted with syngeneic bone marrow cells transduced with either the hGDNF-expressing vector or a corresponding GFP-expressing vector, LV-MSP-Tet-Off-GFP. Suppression of vector gene expression was achieved through administration of Dox in drinking water. To create a toxin-induced Parkinsonian model, mice were injected in two cycles with MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) to yield nigral cell/striatal dopamine loss and behavioral deficits. During the presence of Dox in the drinking water, plasma GDNF was at a basal level, whereas during the absence of Dox, plasma GDNF was significantly elevated, indicating reliable regulation of therapeutic gene expression. Midbrain GDNF levels were altered in parallel, although these did not return completely to basal levels during the periods of Dox withdrawal. Motor activities of the MPTP-Tet-off-hGDNF group were comparable to those of the Tet-off-GFP (subject to no MPTP treatment) group, but substantially better than those of the MPTP-Tet-off-GFP group. Interestingly, the improvement in motor activities was sustained during the Dox-withdrawn periods in MPTP-Tet-off-hGDNF animals. Neuroprotection by therapeutic GDNF expression was further evidenced by significant amelioration of nigral tyrosine hydroxylase loss after both the first and second MPTP treatment cycles. These data suggest that neurotrophic factor expression can be upregulated to achieve efficacy or downregulated in case of off-target effects or adverse events, a feature that may eventually increase the acceptance of this potentially neuroprotective/disease-modifying PD therapy.

1531 related Products with: Regulatable Lentiviral Hematopoietic Stem Cell Gene Therapy in a Mouse Model of Parkinson's Disease.

Antibody to Parkinson Dis Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon DNA (cytosine 5) methyltr Goat Anti-Mouse SAR1, (in Macrophage Colony Stimula Macrophage Colony Stimula Mouse Stem Cell Factor SC Mouse Stromal Cell-Derive Integrin β1 (CD29) Antib Beta Amyloid (42) ELISA K GLP 1 ELISA Kit, Rat Gluc

Related Pathways

  •  
  • No related Items
paperclip

#29534722   // Save this To Up

RPE phagocytic function declines in age-related macular degeneration and is rescued by human umbilical tissue derived cells.

Age-related macular degeneration (AMD) is a leading cause of blindness among the elderly characterized by retinal pigment epithelium (RPE) degeneration with accumulation of abnormal intracellular deposits (lipofuscin) and photoreceptor death. RPE is vital for the retina and integrity of photoreceptors through its phagocytic function which is closely linked to formation of lipofuscin through daily phagocytosis of discarded photoreceptor outer segments (POS). Although phagocytosis has been implicated in AMD, it has not been directly shown to be altered in AMD. RPE phagocytic defect was previously shown to be rescued by subretinal injection of human umbilical tissue derived cells (hUTC) in a rodent model of retinal degeneration (RCS rat) through receptor tyrosine kinase (RTK) ligands and bridge molecules. Here, we examined RPE phagocytic function directly in the RPE from AMD patients and the ability and mechanisms of hUTC to affect phagocytosis in the human RPE.

2803 related Products with: RPE phagocytic function declines in age-related macular degeneration and is rescued by human umbilical tissue derived cells.

Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Goat Anti-Human Laforin ( Macrophage Colony Stimula Macrophage Colony Stimula interleukin 17 receptor C Primary antibody low den NycoPrep™ 1.077, for is Human normal bone and ost Human breast invasive duc Human breast invasive duc Rabbit Anti-intestinal FA

Related Pathways

paperclip

#29505314   // Save this To Up

Neuroprotection of Transplanting Human Umbilical Cord Mesenchymal Stem Cells in a Microbead Induced Ocular Hypertension Rat Model.

The purpose of this study is to investigate the potential therapeutic benefits of intravitreally transplanted human umbilical cord mesenchymal stem cells (UC-MSCs) in an animal model of microbead-injection-induced ocular hypertension (OHT).

2619 related Products with: Neuroprotection of Transplanting Human Umbilical Cord Mesenchymal Stem Cells in a Microbead Induced Ocular Hypertension Rat Model.

Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Human, Rat CHRN Macrophage Colony Stimula Macrophage Colony Stimula Integrin β1 (CD29) Antib TGF beta induced factor 2 Beta Amyloid (42) ELISA K GLP 1 ELISA Kit, Rat Gluc Beta Amyloid (40) ELISA K

Related Pathways

paperclip

#29497380   // Save this To Up

Triple-Gene Therapy for Stroke: A Proof-of-Concept Study in Rats.

Natural brain repair after stroke is extremely limited, and current therapeutic options are even more scarce with no clinical break-through in sight. Despite restricted regeneration in the central nervous system, we have previously proved that human umbilical cord blood mono-nuclear cells (UCB-MC) transduced with adenoviral vectors carrying genes encoding vascular endothelial growth factor (VEGF), glial cell-derived neurotrophic factor (GDNF), and neural cell adhesion molecule (NCAM) successfully rescued neurons in amyotrophic lateral sclerosis and spinal cord injury. This proof-of-principle project was aimed at evaluating the beneficial effects of the same triple-gene approach in stroke. Rats subjected to distal occlusion of the middle cerebral artery were treated intrathecally with a combination of these genes either directly or using our cell-based (UCB-MC) approach. Various techniques and markers were employed to evaluate brain injury and subsequent recovery after treatment. Brain repair was most prominent when therapeutic genes were delivered via adenoviral vector- or UCB-MC-mediated approach. Remodeling of brain cortex in the stroke area was confirmed by reduction of infarct volume and attenuated neural cell death, depletion of astrocytes and microglial cells, and increase in the number of oligodendroglial cells and synaptic proteins expression. These results imply that intrathecal injection of genetically engineered UCB-MC over-expressing therapeutic molecules (VEGF, GDNF, and NCAM) following cerebral blood vessel occlusion might represent a novel avenue for future research into treating stroke.

1774 related Products with: Triple-Gene Therapy for Stroke: A Proof-of-Concept Study in Rats.

DNA (cytosine 5) methyltr Breast invasive ductal ca Multiple lung carcinoma ( Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti ING1B antisense AKT1 (dn) Inducible HIV 1 intergase antigen. MOUSE ANTI BOVINE ROTAVIR Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon

Related Pathways

paperclip

#29477014   // Save this To Up

Glial cell line-derived neurotrophic factor supplementation promotes bovine in vitro oocyte maturation and early embryo development.

Paracrine factors such as glial cell line-derived neurotrophic factor (GDNF), which was originally derived from the supernatants of a rat glioma cell line, play pivotal roles in oocyte maturation and early embryo development in mammals, such as mice, rats, pigs, sheep, and even humans. However, whether GDNF facilitates in vitro oocyte maturation or early embryo development in bovines is not yet known. We show for the first time that GDNF and its receptor, GDNF family receptor alpha-1 (GFRA1), are presented in ovarian follicles at different stages as well as during oocyte maturation and early embryo development. Immunostaining results revealed the subcellular localizations of GDNF and GFRA1 in oocytes throughout follicle development, first in germinal vesicles and during blastocyst embryo stages. The ability of exogenously applied GDNF to promote oocyte maturation and early embryo development was evaluated in culture, where we found that an optimal concentration of 50 ng/mL promotes the maturation of cumulus-oocyte complexes and the nuclei of denuded oocytes as well as the development of embryos after IVF. To further investigate the potential mechanism by which GDNF promotes oocyte maturation, bovine oocytes were treated with morpholinos targeting Gfra1. The suppression of GFRA1 presence blocked endogenous and exogenous GDNF functions, indicating that the effects of GDNF that are essential and beneficial for bovine oocyte maturation and early embryo development occur through this receptor. Furthermore, we show that supplementation with GDNF improves the efficiency of bovine IVF embryo production.

2417 related Products with: Glial cell line-derived neurotrophic factor supplementation promotes bovine in vitro oocyte maturation and early embryo development.

Human Glial Derived Neuro CELLKINES PLATELET DERIVE CELLKINES PLATELET DERIVE Human Brain Derived Neuro Human Stromal Cell-Derive Human Stromal Cell-Derive Mouse Stromal Cell-Derive Mouse Stromal Cell-Derive thymic dendritic cell-der Feline Stromal Cell-Deriv Dog Brain-derived neurotr ELISA Kit for Brain Deriv

Related Pathways

paperclip

#29453972   // Save this To Up

Artemin regulates CXCR4 expression to induce migration and invasion in pancreatic cancer cells through activation of NF-κB signaling.

Pancreatic ductal adenocarcinoma (PDAC) is the most lethal human malignant tumor because of the early onset of local invasion and distant metastasis. Perineural invasion is a prominent characteristic of pancreatic adenocarcinoma, which is a multifactorial process that involves various signaling molecules from different signaling pathways. The glial cell line-derived neurotrophic factor family of ligands was reported to be involved in perineural invasion in pancreatic cancer. Artemin is one member of the glial cell line-derived neurotrophic factor family of ligands. Although Artemin has previously been demonstrated to promote invasiveness of pancreatic cancer, the mechanisms remain poorly understood. In this study, we performed an analysis to determine the effects of Artemin on modulating tumor cell metastatic potential and invasion activity and explored its mechanisms in pancreatic cancer. We indicated that Artemin and CXCR4 were overexpressed in cancer tissues and widely expressed in pancreatic cancer cell lines. We observed that activation of ERK1/2 and Akt in Artemin-treated cells led to enhanced nuclear accumulation of NF-κB, which then induced CXCR4 expression. Through regulation of the expression of CXCR4, Artemin functionally promoted the migration and invasion in pancreatic cancer cells. The present study indicated that Artemin induced CXCR4 expression by activating Akt and ERK 1/2/NF-κB signaling, thereby modulating tumor cell metastatic potential and invasion activity in pancreatic cancer by regulating SDF-1α/CXCR4 axis. Artemin might be an effective and potent therapeutic target for pancreatic cancer metastasis, especially in perineural invasion.

1512 related Products with: Artemin regulates CXCR4 expression to induce migration and invasion in pancreatic cancer cells through activation of NF-κB signaling.

Glucagon ELISA KIT, Rat G NF-kB II Phospho-Specific Top five cancer tissue ar Oral squamous cell cancer Mid advanced stage pancre Pancreatic disease spectr High density pancreatic c Pancreatic cancer tissue Multiple pancreatic cance Pancreatic cancer and nor Pancreatic cancer tissue Pancreatic cancer and nor

Related Pathways

paperclip

#29441947   // Save this To Up

Effect of brefelamide on proliferation of 1321N1 human astrocytoma cells induced by glial cell line-derived neurotrophic factor.

Malignant gliomas are highly resistant to chemotherapy and radiation and more effective options for treatment are urgently needed. We reported previously that the aromatic amide brefelamide, which is isolated from methanolic extracts of the cellular slime molds Dictyostelium giganteum and D. brefeldianum, hinders cellular proliferation in a glioma model utilizing 1321N1 human astrocytoma cells. Herein, we examined the mechanisms underlying the inhibition of 1321N1 cell proliferation by brefelamide. Glial cell line-derived neurotrophic factor (GDNF) was found to enhance the rate of proliferation of serum-free cultured 1321N1 cells, but did not affect proliferation in PC12 cells. Brefelamide pretreatment inhibited GDNF-induced cell proliferation and expression of rearranged during transfection (RET). GDNF enhanced the phosphorylation of extracellular signal-regulated kinase (ERK), AKT, and c-jun-N-terminal kinase (JNK); however, brefelamide pretreatment inhibited these effects. Brefelamide also reduced the expression of GDNF mRNA and GDNF secretion. Together, the findings from this study indicate that brefelamide inhibits the proliferation of 1321N1 cell via several mechanisms including reduced GDNF receptor expression and GDNF secretion, and reduced phosphorylation of ERK, AKT, and JNK.

2571 related Products with: Effect of brefelamide on proliferation of 1321N1 human astrocytoma cells induced by glial cell line-derived neurotrophic factor.

Epidermal Growth Factor ( Epidermal Growth Factor ( Human Glial Derived Neuro Human Brain Derived Neuro Human Stromal Cell-Derive Human Stromal Cell-Derive Macrophage Colony Stimula Macrophage Colony Stimula glial cells missing homol thymic dendritic cell-der Human Cord Blood CD34+ Ce Brain derived Neurotrophi

Related Pathways