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Neuronal differentiation of cryopreserved neural progenitor cells derived from mouse embryonic stem cells.

Embryonic stem cells (ES cells) are developmentally pluripotent cells isolated from pre-implantation mammalian embryos. In cell culture ES cells can be easily differentiated to generate cultures of neural progenitors. We present a simple method for the cryopreservation of these ES-derived neural progenitors. Cryopreserved neural progenitor stocks can be thawed, expanded with FGF2, and differentiated into functional neurons. This method will facilitate studies using ES-derived neural progenitor cells as a cell culture model system for neural development and differentiation. It will also aid studies designed to test the ability of these progenitor cells to functionally engraft and repair damaged neural tissue.

Animals↗

Transplanted adult neural progenitor cells survive, differentiate and reduce motor function impairment in a rodent model of Huntington's disease.

The present study investigated the ability for adult rat neural progenitor cells to survive transplantation, structurally repopulate the striatum and improve motor function in the quinolinic acid (QA) lesion rat model of Huntington's disease. Neural progenitor cells were isolated from the subventricular zone of adult Wistar rats, propagated in culture and labeled with BrdU (50 microM). Fourteen days following QA lesioning, one group of rats (n = 12) received a unilateral injection of adult neural progenitor cells ( approximately 180,000 cells total) in the lesioned striatum, while a second group of rats (n = 10) received a unilateral injection of vehicle only (sham transplant). At the time of transplantation adult neural progenitor cells were phenotypically immature, as demonstrated by SOX2 immunocytochemistry. Eight weeks following transplantation, approximately 12% of BrdU-labeled cells had survived and migrated extensively throughout the lesioned striatum. Double-label immunocytochemical analysis demonstrated that transplanted BrdU-labeled progenitor cells differentiated into either astrocytes, as visualized by GFAP immunocytochemistry, or mature neurons, demonstrated with NeuN. A proportion of BrdU-labeled cells also expressed DARPP-32 and GAD67, specific markers for striatal medium spiny projection neurons and interneurons. Rats transplanted with adult neural progenitor cells also demonstrated a significant reduction in motor function impairment as determined by apomorphine-induced rotational asymmetry and spontaneous exploratory forelimb use when compared to sham transplanted animals. These results demonstrate that adult neural progenitor cells survive transplantation, undergo neuronal differentiation with a proportion of newly generated cells expressing markers characteristic of striatal neurons and reduce functional impairment in the QA lesion model of Huntington's disease.

Analysis of Variance↗

The controlled conversion of human neural progenitor cells derived from foetal ventral mesencephalon into dopaminergic neurons in vitro.

The expansion and differentiation of neural progenitor cells in vitro provides an approach to study the development and differentiation of neurons. The ventral mesencephalic area of the brain is an important source of neural progenitor cells and the differentiated neural progenitor cell has paramount potential for use in transplant therapies such as those used in the treatment of neurodegenerative diseases. Here, the controlled conversion of human foetal progenitor cells derived from ventral mesencephalon into dopaminergic neurons is reported. The immunoreactivity to tyrosine hydroxylase (TH) and levels of dopamine (DA) and its metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), secreted into culture medium, were used to assess dopaminergic neuronal phenotype. Expansion of the neural progenitor cells for 3 weeks in the presence of basic fibroblast growth factor (2 ng/ml) followed by its withdrawal resulted in approximately 60% of cells staining positive for TH, when challenged in concert with brain-derived neurotrophic factor (50 ng/ml), DA (10 microM) and forskolin (10 microM) for a further 3 weeks. A corresponding 41-fold increase in DA and DOPAC was measured in the incubation medium by HPLC. Therefore, the successful conversion of human foetal progenitor cells in vitro resulting in the desired dopaminergic neuronal phenotype, could provide a solution to the problem of limited availability of human foetuses for clinical surgical transplantation therapies, which are currently in progress for the treatment of neurodegenerative diseases such as Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗

Sonic hedgehog regulates adult neural progenitor proliferation in vitro and in vivo.

Neural stem cells exist in the developing and adult nervous systems of all mammals, but the basic mechanisms that control their behavior are not yet well understood. Here, we investigated the role of Sonic hedgehog (Shh), a factor vital for neural development, in regulating adult hippocampal neural stem cells. We found high expression of the Shh receptor Patched in both the adult rat hippocampus and neural progenitor cells isolated from this region. In addition, Shh elicited a strong, dose-dependent proliferative response in progenitors in vitro. Furthermore, adeno-associated viral vector delivery of shh cDNA to the hippocampus elicited a 3.3-fold increase in cell proliferation. Finally, the pharmacological inhibitor of Shh signaling cyclopamine reduced hippocampal neural progenitor proliferation in vivo. This work identifies Shh as a regulator of adult hippocampal neural stem cells.

Animals↗

Transplantation of human neural progenitor cells to the vitreous cavity of the Royal College of Surgeons rat.

Human neural progenitor cells, originally isolated from prenatal donor tissue at 17 weeks of development, were cultured as neurospheres and transplanted to the vitreous cavity of dystrophic Royal College of Surgeons rats with, or without, cyclosporin A immunosuppression. Donor cells were either unlabeled or prelabeled, the latter utilizing incubation with BrdU or adenoviral modification to express green fluorescent protein. Recipients of various ages were examined at 1, 2, and 4 weeks postgrafting. Transplanted human neural progenitor cells survived in the host vitreous for at least 4 weeks and maintained expression of green fluorescent protein for at least 2 weeks. After 2 weeks in vivo, grafted cells differentiated morphologically, coincident with expression of the neuronal marker MAP, indicating mature neuronal differentiation. The extensive intraretinal migration previously shown using rat progenitor cells in the Royal College of Surgeons rat model was not seen in this experiment, suggesting that high levels of neuronal migration may depend at least in part upon species-specific molecular cues. Human neural progenitor cells represent a renewable source of multipotent human cells capable of in vivo neuronal development and a potential means of delivering therapeutic factors intraocularly. Human neural progenitor cells therefore provide a useful tool for studies of neural development and differentiation in the dystrophic eye.

Adenoviridae↗

The endocannabinoid system promotes astroglial differentiation by acting on neural progenitor cells.

Endocannabinoids exert an important neuromodulatory role via presynaptic cannabinoid CB1 receptors and may also participate in the control of neural cell death and survival. The function of the endocannabinoid system has been extensively studied in differentiated neurons, but its potential role in neural progenitor cells remains to be elucidated. Here we show that the CB1 receptor and the endocannabinoid-inactivating enzyme fatty acid amide hydrolase are expressed, both in vitro and in vivo, in postnatal radial glia (RC2+ cells) and in adult nestin type I (nestin(+)GFAP+) neural progenitor cells. Cell culture experiments show that CB1 receptor activation increases progenitor proliferation and differentiation into astroglial cells in vitro. In vivo analysis evidences that, in postnatal CB1(-/-) mouse brain, progenitor proliferation and astrogliogenesis are impaired. Likewise, in adult CB1-deficient mice, neural progenitor proliferation is decreased but is increased in fatty acid amide hydrolase-deficient mice. In addition, endocannabinoid signaling controls neural progenitor differentiation in the adult brain by promoting astroglial differentiation of newly born cells. These results show a novel physiological role of endocannabinoids, which constitute a new family of signaling cues involved in the regulation of neural progenitor cell function.

Amidohydrolases↗

Adult neural progenitor cell grafts survive after acute spinal cord injury and integrate along axonal pathways.

The main rationale for cell-based therapies following spinal cord injury are: (i) replacement of degenerated spinal cord parenchyma by an axon growth supporting scaffold; (ii) remyelination of regenerating axons; and (iii), local delivery of growth promoting molecules. A potential source to meet these requirements is adult neural progenitor cells, which were examined in the present study. Fibroblast growth factor 2-responsive adult spinal cord-derived syngenic neural progenitor cells were either genetically modified in vitro to express green fluorescent protein (GFP) using retroviral vectors or prelabelled with bromodeoxyuridine (BrdU). Neural progenitor cells revealed antigenic properties of neurons and glial cells in vitro confirming their multipotency. This differentiation pattern was unaffected by retroviral transduction. GFP-expressing or BrdU-prelabelled neural progenitor cells were grafted as neurospheres directly into the acutely injured rat cervical spinal cord. Animals with lesions only served as controls. Three weeks postoperatively, grafted neural progenitor cells integrated along axonal profiles surrounding the lesion site. In contrast to observations in culture, grafted neural progenitor cells differentiated only into astro- and oligodendroglial lineages, supporting the notion that the adult spinal cord provides molecular cues for glial, but not for neuronal, differentiation. This study demonstrates that adult neural progenitor cells will survive after transplantation into the acutely injured spinal cord. The observed oligodendroglial and astroglial differentiation and integration along axonal pathways represent important prerequisites for potential remyelination and support of axonal regrowth.

Animals↗

Transplantation of prodrug-converting neural progenitor cells for brain tumor therapy.

Since neural progenitor cells can engraft stably into brain tumors and differentiate along the neuronal and glial line, we tested the hypothesis that transplanted cytosine deaminase (CD)-expressing ST14A cells (an immortalized neural progenitor cell line) can convert locally 5-fluorocytosine (5-FC) into 5-fluorouracil (5-FU) and produce a regression of glioma tumors. ST14A, retrovirally transduced with the E. coli CD gene, showed a strong bystander effect on glioma cells as assessed by in vitro assay. Intracerebral injection of C6 glioma cells generated a rapidly growing tumoral mass. DiI prelabeled ST14A, coinjected into the rat brain with C6 glioma cells, survived in the tumoral mass up to 10 days and their number was not affected by in vivo 5-FC treatment. In contrast, a significant decrease of the glioma tumoral mass (-50%) was observed in 5-FC-treated rats. 5-FC had no effect on the tumor in the absence of CD-expressing ST14A cells. Our results support the feasibility of systems based on intratumoral transplantation of prodrug-converting cells for brain tumor therapy.

Animals↗

NRAGE mediates p38 activation and neural progenitor apoptosis via the bone morphogenetic protein signaling cascade.

Understanding the molecular events that govern neural progenitor lineage commitment, mitotic arrest, and differentiation into functional progeny are germane to our understanding of neocortical development. Members of the family of bone morphogenetic proteins (BMPs) play pivotal roles in regulating neural differentiation and apoptosis during neurogenesis through combined actions involving Smad and TAK1 activation. We demonstrate that BMP signaling is required for the induction of apoptosis of neural progenitors and that NRAGE is a mandatory component of the signaling cascade. NRAGE possesses the ability to bind and function with the TAK1-TAB1-XIAP complex facilitating the activation of p38. Disruption of NRAGE or any other member of the noncanonical signaling cascaded is sufficient to block p38 activation and thus the proapoptotic signals generated through BMP exposure. The function of NRAGE is independent of Smad signaling, but the introduction of a dominant-negative Smad5 also rescues neural progenitor apoptosis, suggesting that both canonical and noncanonical pathways can converge and regulate BMP-mediated apoptosis. Collectively, these results establish NRAGE as an integral component in BMP signaling and clarify its role during neural progenitor development.

Animals↗

Olfactory bulb core is a rich source of neural progenitor and stem cells in adult rodent and human.

The olfactory bulb (OB) core is an extension of the rostral migratory stream and thus is a potential source of neural progenitor and neural stem cells. We characterized in vivo and in vitro neuronal progenitor and neural stem cells in the adult OB core. In mouse and rat, bromodeoxyuridine (BrdU) labeling showed that the OB core accumulates newly replicated cells. Nestin, a neuroepithelial stem cell marker, was enriched in the OB core. BrdU-positive cells were immunolabeled for nestin and TUC4, a marker for early postmitotic neurons. The distributions of cells labeled for BrdU, TUC4, and nestin were similarly concentrated in the OB core. Nestin- and TUC4-positive cells were also found in the OB of young and aged humans. Isolated and cultured OB core cells from adult rat and mouse had the capacity to generate numerous neurospheres. Adult OB core neurospheres were cryopreserved and subsequently cultured. Single cell clonal analysis of neurospheres revealed the capacity for self-renewal and multipotency. Cultured adult OB core cells differentiated into neurons, astrocytes, and oligodendrocytes. Some neurons expressed choline acetlytransferase, substance P, and glutamic acid decarboxylase. Basic fibroblast growth factor potentiated the self-renewal of cells and beta-nerve growth factor stimulated differentiation. OB-derived neural stem cells in coculture with skeletal muscle cells were induced to become neurons expressing choline acetyltransferase and substance P and formed neuromuscular synaptic junctions on myocytes displaying acetylcholinesterase-positive motor end plates. Cocultured OB-derived neural stem cells with myoblast cells also generated nonneural cell progeny. We conclude that the adult mammalian OB core is a reservoir of neural progenitor cells and pluripotent neural stem cells.

Adult↗

The HIV-1 coat protein gp120 regulates CXCR4-mediated signaling in neural progenitor cells.

We demonstrate that hCD4-primed gp120IIIB interacts with CXCR4 receptors expressed by postnatal mouse neural progenitor cells and elicits robust Ca(2+) signals. The chemokine SDF-1 acted as a chemoattractant and a mitogenic stimulus for these neural progenitor cells. Although hCD4/gp120 was not able to produce chemoattraction or increase proliferation, it completely blocked the ability of SDF-1 to produce these effects. Thus, gp120 can act both as an agonist and de facto antagonist of CXCR4-mediated signaling in neural progenitor cells. It is possible that the ability of hCD4/gp120 to block SDF-1 signaling in neural progenitors may contribute to the neuropathological effects of HIV-1.

Animals↗

Promoter-targeted selection and isolation of neural progenitor cells from the adult human ventricular zone.

Adult humans, like their nonhuman mammalian counterparts, harbor persistent neural progenitor cells in the forebrain ventricular lining. In the absence of adequate surface markers, however, these cells have proven difficult to isolate for study. We have previously identified and selected neural progenitor cells from both the fetal and adult rodent ventricular zone (VZ), by sorting forebrain cells transfected with plasmid DNA encoding the gene for green fluorescent protein driven by the early neuronal promoter for Talpha1 tubulin (P/Talpha1:hGFP). We have now extended this approach by purifying both P/Talpha1:hGFP tubulin-defined neuronal progenitors, as well as potentially less committed E/nestin:hGFP-defined neural progenitor cells, from the adult human VZ. The ventricular wall of the temporal horn of the lateral ventricle was dissected from temporal lobes obtained from four adult patients undergoing therapeutic lobectomy. These samples were dissociated, and the cultured cells transduced with either P/Talpha1:hGFP or E/nestin:EGFP plasmid DNA. A week later, the cells were redissociated, selected via fluorescence-activated cell sorting (FACS) on the basis of neural promoter-driven GFP expression, and replated. The majority of these cells expressed the early neuronal protein betaIII-tubulin upon FACS; within the week thereafter, most matured as morphologically evident neurons that coexpressed betaIII-tubulin and microtubule-associated protein (MAP)-2. Many of these neurons had incorporated bromodeoxyuridine in vitro in the days before FACS, indicating their mitogenesis in vitro. Thus, the use of fluorescent transgenes under the control of early neural promoters permits the enrichment of neuronal progenitor cells from the adult human ventricular zone. The specific acquisition, in both purity and number, of residual neural progenitor cells from the adult human brain may now permit hitherto unfeasible studies of both their biology and practical application.

Adult↗

High titer retroviral gene transduction to neural progenitor cells for establishment of donor cells for neural transplantation to parkinsonian model rats.

Neural progenitor cells (NPCs) are expected to be useful donor sources for cell transplantation therapy in Parkinson's disease. However, control of the differentiational lineage, especially into dopaminergic neurons, is still difficult. Thus, genetic modification of NPCs to produce l-dopa is potentially useful. The present study prepared high titer retrovirus carrying human tyrosine hydroxylase-1 (HTH-1) gene. HTH-1 gene could be efficiently transduced into NPCs obtained from the E12.5 rat mesencephalon. This retroviral gene transduction caused no apparent changes in survival, proliferation, or differentiation. In vitro, HTH-1 gene-transduced NPCs released little l-dopa and addition of tetrahydrobiopterin, the cofactor of tyrosine hydroxylase, was required for production of l-dopa. In vivo, three of seven hemi-parkinsonian model rats that received HTH-1 gene-transduced donor NPCs achieved functional recovery. High titer retroviral vector for gene transduction could be used to prepare NPCs for transplantation to hemi-parkinsonian model rats. However, functional recovery after transplantation of HTH-1 gene-transduced NPCs was incomplete.

Animals↗

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗

In vitro expansion of a multipotent population of human neural progenitor cells.

The isolation and expansion of human neural progenitor cells have important potential clinical applications, because these cells may be used as graft material in cell therapies to regenerate tissue and/or function in patients with central nervous system (CNS) disorders. This paper describes a continuously dividing multipotent population of progenitor cells in the human embryonic forebrain that can be propagated in vitro. These cells can be maintained and expanded using a serum-free defined medium containing basic fibroblast growth factor (bFGF), leukemia inhibitory factor (LIF), and epidermal growth factor (EGF). Using these three factors, the cell cultures expand and remain multipotent for at least 1 year in vitro. This period of expansion results in a 10(7)-fold increase of this heterogeneous population of cells. Upon differentiation, they form neurons, astrocytes, and oligodendrocytes, the three main phenotypes in the CNS. Moreover, GABA-immunoreactive and tyrosine hydroxylase-immunoreactive neurons can be identified. These results demonstrate the feasibility of long-term in vitro expansion of human neural progenitor cells. The advantages of such a population of neural precursors for allogeneic transplantation include the ability to provide an expandable, well-characterized, defined cell source which can form specific neuronal or glial subtypes.

Brain↗

Chemokine receptors are expressed widely by embryonic and adult neural progenitor cells.

We investigated the expression and functions of chemokine receptors in neural progenitor cells isolated from embryonic and adult mice. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis demonstrated mRNA expression for most known chemokine receptors in neural progenitor cells grown as neurospheres from embryonic (E17) and adult (4-week-old) mice. The expression of CXCR4 receptors was demonstrated further in E17 neurospheres using immunohistochemistry, in situ hybridization, Northern blot analysis and fura-2-based Ca(2+) imaging. Most neurospheres grown from E17 mice responded to stromal cell-derived factor-1 (SDF-1/CXCL12) in Ca(2+) imaging studies. In addition, immunohistochemical studies demonstrated that these neurospheres consisted of dividing cells that uniformly colocalized nestin and CXCR4 receptors. Differentiation of E17 neurospheres yielded astrocytes and neurons exhibiting several different phenotypes, including expression of calbindin, calretinin, gamma-aminobutyric acid (GABA), and glutamate, and many also coexpressed CXCR4 receptors. In addition, neurospheres grown from the subventricular zone (SVZ) of 4-week-old mice exhibited large increases in Ca(2+) in response to CXCL12 and several other chemokines. In comparison, neurospheres prepared from olfactory bulb of adult mice exhibited only small Ca(2+) responses to CXCL12, whereas neurospheres prepared from hippocampus were insensitive to CXCL12, although they did respond to other chemokines. Investigations designed to investigate whether CXCL12 can act as a chemoattractant demonstrated that cells dissociated from E17 or adult SVZ neurospheres migrated toward an CXCL12 gradient and this was blocked by the CXCR4 antagonist AMD3100. These results illustrate widespread chemokine sensitivity of embryonic and adult neural progenitor cells and support the view that chemokines may be of general importance in control of progenitor cell migration in embryonic and adult brain.

Animals↗

Conditionally immortalized neural progenitor cell lines integrate and differentiate after grafting to the adult rat striatum. A combined autoradiographic and electron microscopic study.

Neural progenitor cell lines, generated by conditional immortalization from the embryonic CNS, have previously been shown to survive and integrate after transplantation to the adult brain. The present study was designed to investigate the in vivo differentiation and morphological features of grafted neural progenitors using combined autoradiography and transmission electron microscopy of two temperature-sensitive neural progenitor cell lines, HiB5 and ST14A, labeled with 3H-thymidine prior to grafting. Two weeks after transplantation to the striatum the cells were found dispersed over an area extending about 1.5 mm from the injection site. Labeled cells located within the myelinated fiber bundles of the internal capsule were closely associated with myelinated axons and presented profiles similar to oligodendrocytes, while most of the grafted cells in the grey matter had morphological features of astroglia. Some labeled cells occurred also in close association with small blood vessels, morphologically resembling host pericytes. The results show that the immortalized neural progenitors can differentiate into mature glial cells, including astrocytes, oligodendrocytes and pericytes, after implantation into the adult striatum. The ability of the cells to become fully integrated with the resident glial population suggests that they will be highly useful as vehicles for intracerebral transgene expression in ex vivo gene transfer.

Animals↗

Neural progenitor cells promote corticospinal axon growth in organotypic co-cultures.

The CNS is limited in regeneration following injury in adult mammals. Recent studies show that the transplantation of the neuronal progenitor cells is useful in promoting regeneration. However, the mechanisms of action of the transplanted neural progenitor cells have not been clarified. In this study, we used organotypic co-cultures with neonatal brain cortex and spinal cord as an in vitro assay system for assessing the factors that regulate corticospinal axonal growth. Our results show that the transplantation of neural progenitor cells enhanced corticospinal axon growth in these co-cultures. In addition, neural progenitor cell conditioned medium also significantly promoted axonal growth. These findings strongly suggest that factors derived from neural progenitor cells participate in the effect on axonal growth.

Age Factors↗