Journal articles: 'Neuronal progenitors'

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Shih, Hung-Yu, Chia-Wei Chang, Yi-Chieh Chen, and Yi-Chuan Cheng. "Identification of the Time Period during Which BMP Signaling Regulates Proliferation of Neural Progenitor Cells in Zebrafish." International Journal of Molecular Sciences 24, no. 2 (January 15, 2023): 1733. http://dx.doi.org/10.3390/ijms24021733.

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Bone morphogenetic protein (BMP) signaling regulates neural induction, neuronal specification, and neuronal differentiation. However, the role of BMP signaling in neural progenitors remains unclear. This is because interruption of BMP signaling before or during neural induction causes severe effects on subsequent neural developmental processes. To examine the role of BMP signaling in the development of neural progenitors in zebrafish, we bypassed the effect of BMP signaling on neural induction and suppressed BMP signaling at different time points during gastrulation using a temporally controlled transgenic line carrying a dominant-negative form of Bmp receptor type 1aa and a chemical inhibitor of BMP signaling, DMH1. Inhibiting BMP signaling from 8 hpf could bypass BMP regulation on neural induction, induce the number of proliferating neural progenitors, and reduce the number of neuronal precursors. Inhibiting BMP signaling upregulates the expression of the Notch downstream gene hairy/E(spl)-related 2 (her2). Inhibiting Notch signaling or knocking down the Her2 function reduced neural progenitor proliferation, whereas inactivating BMP signaling in Notch-Her2 deficient background restored the number of proliferating neural progenitors. These results reveal the time window for the proliferation of neural progenitors during zebrafish development and a fine balance between BMP and Notch signaling in regulating the proliferation of neural progenitor cells.

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Wang, D. D., D. D. Krueger, and A. Bordey. "Biophysical Properties and Ionic Signature of Neuronal Progenitors of the Postnatal Subventricular Zone In Situ." Journal of Neurophysiology 90, no. 4 (October 2003): 2291–302. http://dx.doi.org/10.1152/jn.01116.2002.

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Previous studies have reported the presence of neuronal progenitors in the subventricular zone (SVZ) and rostral migratory stream (RMS) of the postnatal mammalian brain. Although many studies have examined the survival and migration of progenitors after transplantation and the factors influencing their proliferation or differentiation, no information is available on the electrophysiological properties of these progenitors in a near-intact environment. Thus we performed whole cell and cell-attached patch-clamp recordings of progenitors in brain slices containing either the SVZ or the RMS from postnatal day 15 to day 25 mice. Both regions displayed strong immunoreactivity for nestin and neuron-specific class III β-tubulin, and recorded cells displayed a morphology typical of the neuronal progenitors known to migrate throughout the SVZ and RMS to the olfactory bulb. Recorded progenitors had depolarized zero-current resting potentials (mean more depolarized than –28 mV), very high input resistances (about 4 GΩ), and lacked action potentials. Using the reversal potential of K+ currents through a cell-attached patch a mean resting potential of –59 mV was estimated. Recorded progenitors displayed Ca2+-dependent K+ currents and TEA-sensitive-delayed rectifying K+ (KDR) currents, but lacked inward K+ currents and transient outward K+ currents. KDR currents displayed classical kinetics and were also sensitive to 4-aminopyridine and α-dendrotoxin, a blocker of Kv1 channels. Na+ currents were found in about 60% of the SVZ neuronal progenitors. No developmental changes were observed in the passive membrane properties and current profile of neuronal progenitors. Together these data suggest that SVZ neuronal progenitors display passive membrane properties and an ionic signature distinct from that of cultured SVZ neuronal progenitors and mature neurons.

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Turrero García, Miguel, José-Manuel Baizabal, Diana N. Tran, Rui Peixoto, Wengang Wang, Yajun Xie, Manal A. Adam, et al. "Transcriptional regulation of MGE progenitor proliferation by PRDM16 controls cortical GABAergic interneuron production." Development 147, no. 22 (October 15, 2020): dev187526. http://dx.doi.org/10.1242/dev.187526.

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ABSTRACTThe mammalian cortex is populated by neurons derived from neural progenitors located throughout the embryonic telencephalon. Excitatory neurons are derived from the dorsal telencephalon, whereas inhibitory interneurons are generated in its ventral portion. The transcriptional regulator PRDM16 is expressed by radial glia, neural progenitors present in both regions; however, its mechanisms of action are still not fully understood. It is unclear whether PRDM16 plays a similar role in neurogenesis in both dorsal and ventral progenitor lineages and, if so, whether it regulates common or unique networks of genes. Here, we show that Prdm16 expression in mouse medial ganglionic eminence (MGE) progenitors is required for maintaining their proliferative capacity and for the production of proper numbers of forebrain GABAergic interneurons. PRDM16 binds to cis-regulatory elements and represses the expression of region-specific neuronal differentiation genes, thereby controlling the timing of neuronal maturation. PRDM16 regulates convergent developmental gene expression programs in the cortex and MGE, which utilize both common and region-specific sets of genes to control the proliferative capacity of neural progenitors, ensuring the generation of correct numbers of cortical neurons.

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Ruan, Xiangbin, Bowei Kang, Cai Qi, Wenhe Lin, Jingshu Wang, and Xiaochang Zhang. "Progenitor cell diversity in the developing mouse neocortex." Proceedings of the National Academy of Sciences 118, no. 10 (March 1, 2021): e2018866118. http://dx.doi.org/10.1073/pnas.2018866118.

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In the mammalian neocortex, projection neuron types are sequentially generated by the same pool of neural progenitors. How neuron type specification is related to developmental timing remains unclear. To determine whether temporal gene expression in neural progenitors correlates with neuron type specification, we performed single-cell RNA sequencing (scRNA-Seq) analysis of the developing mouse neocortex. We uncovered neuroepithelial cell enriched genes such as Hmga2 and Ccnd1 when compared to radial glial cells (RGCs). RGCs display dynamic gene expression over time; for instance, early RGCs express higher levels of Hes5, and late RGCs show higher expression of Pou3f2. Interestingly, intermediate progenitor cell marker gene Eomes coexpresses temporally with known neuronal identity genes at different developmental stages, though mostly in postmitotic cells. Our results delineate neural progenitor cell diversity in the developing mouse neocortex and support that neuronal identity genes are transcriptionally evident in Eomes-positive cells.

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Findlay, Quan, Kiryu K. Yap, Annette J. Bergner, Heather M. Young, and Lincon A. Stamp. "Enteric neural progenitors are more efficient than brain-derived progenitors at generating neurons in the colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 7 (October 1, 2014): G741—G748. http://dx.doi.org/10.1152/ajpgi.00225.2014.

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Gut motility disorders can result from an absent, damaged, or dysfunctional enteric nervous system (ENS). Cell therapy is an exciting prospect to treat these enteric neuropathies and restore gut motility. Previous studies have examined a variety of sources of stem/progenitor cells, but the ability of different sources of cells to generate enteric neurons has not been directly compared. It is important to identify the source of stem/progenitor cells that is best at colonizing the bowel and generating neurons following transplantation. The aim of this study was to compare the ability of central nervous system (CNS) progenitors and ENS progenitors to colonize the colon and differentiate into neurons. Genetically labeled CNS- and ENS-derived progenitors were cocultured with aneural explants of embryonic mouse colon for 1 or 2.5 wk to assess their migratory, proliferative, and differentiation capacities, and survival, in the embryonic gut environment. Both progenitor cell populations were transplanted in the postnatal colon of mice in vivo for 4 wk before they were analyzed for migration and differentiation using immunohistochemistry. ENS-derived progenitors migrated further than CNS-derived cells in both embryonic and postnatal gut environments. ENS-derived progenitors also gave rise to more neurons than their CNS-derived counterparts. Furthermore, neurons derived from ENS progenitors clustered together in ganglia, whereas CNS-derived neurons were mostly solitary. We conclude that, within the gut environment, ENS-derived progenitors show superior migration, proliferation, and neuronal differentiation compared with CNS progenitors.

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Nagler, Arnon, Hadar Arien-Zakay, Shimon Lecht, Hanan Galski, and Philip Lazarovici. "Nerve Growth Factor-Responsive Neuronal Progenitors From Human Umbilical Cord Blood." Blood 114, no. 22 (November 20, 2009): 4601. http://dx.doi.org/10.1182/blood.v114.22.4601.4601.

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Abstract Abstract 4601 Background Nerve growth factor (NGF) is a well characterized neurotrophin required for the survival and differentiation of a variety of cell types in the peripheral and central nervous system. Over the last decade, many studies have demonstrated the physiological role of NGF in proliferation, differentiation and activation of different hematopoietic cells. Hematopoietic progenitors from bone marrow, umbilical cord blood and peripheral blood were found to be responsive to the actions of NGF. Furthermore, bone marrow stromal cells produce and respond to NGF during different steps of normal hematopoiesis. Results In this study, we describe a population of collagen-adherent, CD49a/b (á1/2 integrin receptors) and nestin-positive human umbilical cord blood derived progenitors. The identity of these cells was established as positive for the mesenchymal markers: CD13, CD29, CD44, CD49a,b, CD49e, CD73, CD105 and vimentin and negative for the hematopoietic markers: CD34, CD49c, CD49d, CD62e, CD62p, CD106, CD117, CD133, CD235a, HLA-DRB4 and HAS1, using Affimatrix™ human DNA chip technology, immunomagnetic sorting and Western blotting approaches. The NGF- receptor, TrkA, was found to be expressed upon isolation of these progenitors, but was gradually down-regulated upon 14 days growth in culture, as measured by mRNA, protein expression and binding properties. However, continuous presense of NGF in the culture media preserved the TrkA receptors expression. The pan-neurotrophin NGF receptor p75NTR, belonging to the TNF family of cell-death receptors, was not detected in the progenitors at any time. The effect of NGF on the cord blood progenitors global gene expression indicated highly increased expression of 170 genes, 24 and 20% of which were related to neuronal proliferation (NEK1, cyclin B1, EGR4, LGN, GATA6) or differentiation (AP2, Neurogenic differentiation factor 2, lamin B1, Ca(2+)-activated Cl- channel, Kv channel, GABA-A alpha 5 receptor, D2 dopamine receptor, neuropeptides precursor), respectively and strong reduction in the expression of 58 genes, 35% of which were hematopoiesis-related (CD7, T cell receptor alpha, interleukin 21 receptor, natural killer cell transcript 4, HLA-G, complement component1, defensin alpha1). Furthermore, upon treatment with NGF, the progenitors expressed a neuronal-like phenotype as evaluated by measurements of long neurite outgrowths and various developmental neuronal markers expression (MAP-2, NeuN neurofillament-160, beta-tubulin III, neuron specific enolase). These findings strongly suggest NGF-induced reprogramming of the cord blood derived progenitors towards neuronal differentiation commitment. The progenitors were also found to confer ∼35% neuroprotection to neurons exposed to an ischemic damage by a “bystander” effect mechanism, which includes the increased autocrine secretion of NGF and activation of TrkA receptors in the insulted neurons. Conclusions These results suggest an important role for NGF in regulating human umbilical cord blood neuronal progenitor's growth and reprogramming towards neuronal differentiation. In view of the broad spectrum of possible uses of cord blood in transplantations, we may also suggest that human umbilical cord blood and/or derived NGF-responsive progenitors may serve as a useful source of neuronal cells for cell therapy of neuropathological disorders. Disclosures: No relevant conflicts of interest to declare.

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Antel, Jack P., Josephine Nalbantoglu, and André Olivier. "Neuronal progenitors—learning from the hippocampus." Nature Medicine 6, no. 3 (March 2000): 249–50. http://dx.doi.org/10.1038/73076.

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Dubreuil, V., M. Hirsch, A. Pattyn, J. Brunet, and C. Goridis. "The Phox2b transcription factor coordinately regulates neuronal cell cycle exit and identity." Development 127, no. 23 (December 1, 2000): 5191–201. http://dx.doi.org/10.1242/dev.127.23.5191.

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In the vertebrate neural tube, cell cycle exit of neuronal progenitors is accompanied by the expression of transcription factors that define their generic and sub-type specific properties, but how the regulation of cell cycle withdrawal intersects with that of cell fate determination is poorly understood. Here we show by both loss- and gain-of-function experiments that the neuronal-subtype-specific homeodomain transcription factor Phox2b drives progenitor cells to become post-mitotic. In the absence of Phox2b, post-mitotic neuronal precursors are not generated in proper numbers. Conversely, forced expression of Phox2b in the embryonic chick spinal cord drives ventricular zone progenitors to become post-mitotic neurons and to relocate to the mantle layer. In the neurons thus generated, ectopic expression of Phox2b is sufficient to initiate a programme of motor neuronal differentiation characterised by expression of Islet1 and of the cholinergic transmitter phenotype, in line with our previous results showing that Phox2b is an essential determinant of cranial motor neurons. These results suggest that Phox2b coordinates quantitative and qualitative aspects of neurogenesis, thus ensuring that neurons of the correct phenotype are generated in proper numbers at the appropriate times and locations.

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Mikhailov, Andrey, and Yoshiyuki Sankai. "Apoptosis in Postmortal Tissues of Goat Spinal Cords and Survival of Resident Neural Progenitors." International Journal of Molecular Sciences 25, no. 9 (April 25, 2024): 4683. http://dx.doi.org/10.3390/ijms25094683.

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Growing demand for therapeutic tissue repair recurrently focusses scientists’ attention on critical assessment of postmortal collection of live cells, especially stem cells. Our study aimed to assess the survival of neuronal progenitors in postmortal spinal cord and their differentiation potential. Postmortal samples of spinal cords were obtained from human-sized animals (goats) at 6, 12, 24, 36, and 54 h after slaughter. Samples were studied by immunohistology, differentiation assay, Western blot and flow cytometry for the presence and location of GD2-positive neural progenitors and their susceptibility to cell death. TUNEL staining of the goat spinal cord samples over 6–54 h postmortem revealed no difference in the number of positive cells per cross-section. Many TUNEL-positive cells were located in the gray commissure around the central canal of the spinal cord; no increase in TUNEL-positive cells was recorded in either posterior or anterior horns of the gray matter where many GD2-positive neural progenitors can be found. The active caspase 3 amount as measured by Western blot at the same intervals was moderately increasing over time. Neuronal cells were enriched by magnetic separation with antibodies against CD24; among them, the GD2-positive neural progenitor subpopulation did not overlap with apoptotic cells having high pan-caspase activity. Apoptotic cell death events are relatively rare in postmortal spinal cords and are not increased in areas of the neural progenitor cell’s location, within measured postmortal intervals, or among the CD24/GD2-positive cells. Data from our study suggest postmortal spinal cords as a valuable source for harvesting highly viable allogenic neural progenitor cells.

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McConnell, SK, and CE Kaznowski. "Cell cycle dependence of laminar determination in developing neocortex." Science 254, no. 5029 (October 11, 1991): 282–85. http://dx.doi.org/10.1126/science.254.5029.282.

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The neocortex is patterned in layers of neurons that are generated in an orderly sequence during development. This correlation between cell birthday and laminar fate prompted an examination of how neuronal phenotypes are determined in the developing cortex. At various times after labeling with [3H]thymidine, embryonic progenitor cells were transplanted into older host brains. The laminar fate of transplanted neurons correlates with the position of their progenitors in the cell cycle at the time of transplantation. Daughters of cells transplanted in S-phase migrate to layer 2/3, as do host neurons. Progenitors transplanted later in the cell cycle, however, produce daughters that are committed to their normal, deep-layer fates. Thus, environmental factors are important determinants of laminar fate, but embryonic progenitors undergo cyclical changes in their ability to respond to such cues.

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Petridou, Eleni, and Leanne Godinho. "Cellular and Molecular Determinants of Retinal Cell Fate." Annual Review of Vision Science 8, no. 1 (September 15, 2022): 79–99. http://dx.doi.org/10.1146/annurev-vision-100820-103154.

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The vertebrate retina is regarded as a simple part of the central nervous system (CNS) and thus amenable to investigations of the determinants of cell fate. Its five neuronal cell classes and one glial cell class all derive from a common pool of progenitors. Here we review how each cell class is generated. Retinal progenitors progress through different competence states, in each of which they generate only a small repertoire of cell classes. The intrinsic state of the progenitor is determined by the complement of transcription factors it expresses. Thus, although progenitors are multipotent, there is a bias in the types of fates they generate during any particular time window. Overlying these competence states are stochastic mechanisms that influence fate decisions. These mechanisms are determined by a weighted set of probabilities based on the abundance of a cell class in the retina. Deterministic mechanisms also operate, especially late in development, when preprogrammed progenitors solely generate specific fates.

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Tietjen, Ian, Jason M. Rihel, Yanxiang Cao, Georgy Koentges, Lisa Zakhary, and Catherine Dulac. "Single-Cell Transcriptional Analysis of Neuronal Progenitors." Neuron 38, no. 2 (April 2003): 161–75. http://dx.doi.org/10.1016/s0896-6273(03)00229-0.

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Lauter, Gilbert, Andrea Coschiera, Masahito Yoshihara, Debora Sugiaman-Trapman, Sini Ezer, Shalini Sethurathinam, Shintaro Katayama, Juha Kere, and Peter Swoboda. "Differentiation of ciliated human midbrain-derived LUHMES neurons." Journal of Cell Science 133, no. 21 (October 28, 2020): jcs249789. http://dx.doi.org/10.1242/jcs.249789.

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ABSTRACTMany human cell types are ciliated, including neural progenitors and differentiated neurons. Ciliopathies are characterized by defective cilia and comprise various disease states, including brain phenotypes, where the underlying biological pathways are largely unknown. Our understanding of neuronal cilia is rudimentary, and an easy-to-maintain, ciliated human neuronal cell model is absent. The Lund human mesencephalic (LUHMES) cell line is a ciliated neuronal cell line derived from human fetal mesencephalon. LUHMES cells can easily be maintained and differentiated into mature, functional neurons within one week. They have a single primary cilium as proliferating progenitor cells and as postmitotic, differentiating neurons. These developmental stages are completely separable within one day of culture condition change. The sonic hedgehog (SHH) signaling pathway is active in differentiating LUHMES neurons. RNA-sequencing timecourse analyses reveal molecular pathways and gene-regulatory networks critical for ciliogenesis and axon outgrowth at the interface between progenitor cell proliferation, polarization and neuronal differentiation. Gene expression dynamics of cultured LUHMES neurons faithfully mimic the corresponding in vivo dynamics of human fetal midbrain. In LUHMES cells, neuronal cilia biology can be investigated from proliferation through differentiation to mature neurons.

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Camp, J. Gray, Farhath Badsha, Marta Florio, Sabina Kanton, Tobias Gerber, Michaela Wilsch-Bräuninger, Eric Lewitus, et al. "Human cerebral organoids recapitulate gene expression programs of fetal neocortex development." Proceedings of the National Academy of Sciences 112, no. 51 (December 7, 2015): 15672–77. http://dx.doi.org/10.1073/pnas.1520760112.

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Cerebral organoids—3D cultures of human cerebral tissue derived from pluripotent stem cells—have emerged as models of human cortical development. However, the extent to which in vitro organoid systems recapitulate neural progenitor cell proliferation and neuronal differentiation programs observed in vivo remains unclear. Here we use single-cell RNA sequencing (scRNA-seq) to dissect and compare cell composition and progenitor-to-neuron lineage relationships in human cerebral organoids and fetal neocortex. Covariation network analysis using the fetal neocortex data reveals known and previously unidentified interactions among genes central to neural progenitor proliferation and neuronal differentiation. In the organoid, we detect diverse progenitors and differentiated cell types of neuronal and mesenchymal lineages and identify cells that derived from regions resembling the fetal neocortex. We find that these organoid cortical cells use gene expression programs remarkably similar to those of the fetal tissue to organize into cerebral cortex-like regions. Our comparison of in vivo and in vitro cortical single-cell transcriptomes illuminates the genetic features underlying human cortical development that can be studied in organoid cultures.

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Hill, Justin, and John Cave. "Targeting the vasculature to improve neural progenitor transplant survival." Translational Neuroscience 6, no. 1 (January 1, 2015): 162–67. http://dx.doi.org/10.1515/tnsci-2015-0016.

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AbstractNeural progenitor transplantation is a promising therapeutic option for several neurological diseases and injuries. In nearly all human clinical trials and animal models that have tested this strategy, the low survival rate of progenitors after engraftment remains a significant challenge to overcome. Developing methods to improve the survival rate will reduce the number of cells required for transplant and will likely enhance functional improvements produced by the procedure. Here we briefly review the close relationship between the blood vasculature and neural progenitors in both the embryo and adult nervous system. We also discuss previous studies that have explored the role of the vasculature and hypoxic pre-conditioning in neural transplants. From these studies, we suggest that hypoxic pre-conditioning of a progenitor pool containing both neural and endothelial cells will improve engrafted transplanted neuronal survival rates.

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Pittack, C., M. Jones, and T. A. Reh. "Basic fibroblast growth factor induces retinal pigment epithelium to generate neural retina in vitro." Development 113, no. 2 (October 1, 1991): 577–88. http://dx.doi.org/10.1242/dev.113.2.577.

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During embryogenesis, the cells of the eye primordium are initially capable of giving rise to either neural retina or pigmented epithelium (PE), but become restricted to one of these potential cell fates. However, following surgical removal of the retina in embryonic chicks and larval amphibians, new neural retina is generated by the transdifferentiation, or phenotypic switching, of PE cells into neuronal progenitors. A recent study has shown that basic fibroblast growth factor (bFGF) stimulates this process in chicks in vivo. To characterize further the mechanisms by which this factor regulates the phenotype of retinal tissues, we added bFGF to enzymatically dissociated chick embryo PE. We found that bFGF stimulated proliferation and caused several morphological changes in the PE, including the loss of pigmentation; however, no transdifferentiation to neuronal phenotypes was observed. By contrast, when small sheets of PE were cultured as aggregates on a shaker device, preventing flattening and spreading on the substratum, we found that a large number of retinal progenitor cells were generated from the PE treated with bFGF. These results indicate that bFGF promotes retinal regeneration in vitro, as well as in ovo, and suggest that the ability of chick PE to undergo transdifferentiation to neuronal progenitors appears to be dependent on the physical configuration of the cells.

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Andrews, Madeline G., and Caroline A. Pearson. "Toward an understanding of glucose metabolism in radial glial biology and brain development." Life Science Alliance 7, no. 1 (October 5, 2023): e202302193. http://dx.doi.org/10.26508/lsa.202302193.

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Decades of research have sought to determine the intrinsic and extrinsic mechanisms underpinning the regulation of neural progenitor maintenance and differentiation. A series of precise temporal transitions within progenitor cell populations generates all the appropriate neural cell types while maintaining a pool of self-renewing progenitors throughout embryogenesis. Recent technological advances have enabled us to gain new insights at the single-cell level, revealing an interplay between metabolic state and developmental progression that impacts the timing of proliferation and neurogenesis. This can have long-term consequences for the developing brain’s neuronal specification, maturation state, and organization. Furthermore, these studies have highlighted the need to reassess the instructive role of glucose metabolism in determining progenitor cell division, differentiation, and fate. This review focuses on glucose metabolism (glycolysis) in cortical progenitor cells and the emerging focus on glycolysis during neurogenic transitions. Furthermore, we discuss how the field can learn from other biological systems to improve our understanding of the spatial and temporal changes in glycolysis in progenitors and evaluate functional neurological outcomes.

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Rusu, Mugurel, Valentina Mănoiu, Nicolae Mirancea, and Gheorghe Nini. "Quiescent satellite glial cells of the adult trigeminal ganglion." Open Medicine 9, no. 3 (June 1, 2014): 500–504. http://dx.doi.org/10.2478/s11536-013-0285-z.

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AbstractSensory ganglia comprise functional units built up by neurons and satellite glial cells (SGCs). In animal species there was proven the presence of neuronoglial progenitor cells in adult samples. Such neural crest-derived progenitors were found in immunohistochemistry (IHC). These findings were not previously documented in transmission electron microscopy (TEM). It was thus aimed to assess in TEM if cells of the human adult trigeminal ganglion indeed have ultrastructural features to qualify for a progenitor, or quiescent phenotype. Trigeminal ganglia were obtained from fifteen adult donor cadavers. In TEM, cells with heterochromatic nuclei, a pancytoplasmic content of free ribosomes, few perinuclear mitochondria, poor developed endoplasmic reticulum, lack of Golgi complexes and membrane trafficking specializations, were found included in the neuronal envelopes built-up by SGCs. The ultrastructural pattern was strongly suggestive for these cells being quiescent progenitors. However, further experiments should correlate the morphologic and immune phenotypes of such cells.

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Davidoff, Michail S., Ralf Middendorff, Grigori Enikolopov, Dieter Riethmacher, Adolf F. Holstein, and Dieter Müller. "Progenitor cells of the testosterone-producing Leydig cells revealed." Journal of Cell Biology 167, no. 5 (November 29, 2004): 935–44. http://dx.doi.org/10.1083/jcb.200409107.

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The cells responsible for production of the male sex hormone testosterone, the Leydig cells of the testis, are post-mitotic cells with neuroendocrine characteristics. Their origin during ontogeny and regeneration processes is still a matter of debate. Here, we show that cells of testicular blood vessels, namely vascular smooth muscle cells and pericytes, are the progenitors of Leydig cells. Resembling stem cells of the nervous system, the Leydig cell progenitors are characterized by the expression of nestin. Using an in vivo model to induce and monitor the synchronized generation of a completely new Leydig cell population in adult rats, we demonstrate specific proliferation of vascular progenitors and their subsequent transdifferentiation into steroidogenic Leydig cells which, in addition, rapidly acquire neuronal and glial properties. These findings, shown to be representative also for ontogenetic Leydig cell formation and for the human testis, provide further evidence that cellular components of blood vessels can act as progenitor cells for organogenesis and repair.

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Guo, Duancheng, Yanghui Qu, Yijun Yang, and Zeng-Jie Yang. "Medulloblastoma cells resemble neuronal progenitors in their differentiation." Molecular & Cellular Oncology 7, no. 6 (September 5, 2020): 1810514. http://dx.doi.org/10.1080/23723556.2020.1810514.

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Komine, Okiru, Mai Nagaoka, Yuichi Hiraoka, Mikio Hoshino, Yoshiya Kawaguchi, Warren S. Pear, and Kohichi Tanaka. "RBP-J promotes the maturation of neuronal progenitors." Developmental Biology 354, no. 1 (June 2011): 44–54. http://dx.doi.org/10.1016/j.ydbio.2011.03.020.

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Lu, Zhenjie, Michael R. Elliott, Yubo Chen, James T. Walsh, Alexander L. Klibanov, Kodi S. Ravichandran, and Jonathan Kipnis. "Phagocytic activity of neuronal progenitors regulates adult neurogenesis." Nature Cell Biology 13, no. 9 (July 31, 2011): 1076–83. http://dx.doi.org/10.1038/ncb2299.

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Vukicevic, Vladimir, Maria F. Rubin de Celis, Gabriela Diaz-Valencia, Stefan R. Bornstein, and Monika Ehrhart-Bornstein. "Modulation of Dopaminergic Neuronal Differentiation from Sympathoadrenal Progenitors." Journal of Molecular Neuroscience 48, no. 2 (March 25, 2012): 420–26. http://dx.doi.org/10.1007/s12031-012-9746-0.

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Rosario, C. M., B. D. Yandava, B. Kosaras, D. Zurakowski, R. L. Sidman, and E. Y. Snyder. "Differentiation of engrafted multipotent neural progenitors towards replacement of missing granule neurons in meander tail cerebellum may help determine the locus of mutant gene action." Development 124, no. 21 (November 1, 1997): 4213–24. http://dx.doi.org/10.1242/dev.124.21.4213.

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Previously we observed that stable clones of multipotent neural progenitor cells, initially isolated and propagated from the external granular layer of newborn wild-type mouse cerebellum, could participate appropriately in cerebellar development when reimplanted into the external granular layer of normal mice. Donor cells could reintegrate and differentiate into neurons (including granule cells) and/or glia consistent with their site of engraftment. These findings suggested that progenitors might be useful for cellular replacement in models of aberrant neural development or neurodegeneration. We tested this hypothesis by implanting clonally related multipotent progenitors into the external granular layer of newborn meander tail mice (gene symbol=mea). mea is an autosomal recessive mutation characterized principally by the failure of granule cells to develop in the cerebellar anterior lobe; the mechanism is unknown. We report that approximately 75% of progenitors transplanted into the granuloprival anterior lobe of neonatal mea mutants differentiated into granule cells, partially replacing or augmenting that largely absent neuronal population in the internal granular layer of the mature meander tail anterior lobe. (The ostensibly ‘normal’ meander tail posterior lobe also benefited from repletion of a more subtle granule cell deficiency.) Donor-derived neurons were well-integrated within the neuropil, suggesting that these progenitors' developmental programs for granule cell differentiation were unperturbed. These observations permitted several conclusions. (1) That exogenous progenitors could survive transplantation into affected regions of neonatal meander tail cerebellum and differentiate into the deficient cell type suggested that the microenvironment was not inimical to granule cell development. Rather it suggested that mea's deleterious action is intrinsic to the external granular layer cell. (Any cell-extrinsic actions--albeit unlikely--had to be restricted to readily circumventable prenatal events.) This study, therefore, offers a paradigm for using progenitors to help determine the site of action of other mutant genes or to test hypotheses regarding the pathophysiology underlying other anomalies. (2) In the regions most deficient in neurons, a neuronal phenotype was pursued in preference to other potential cell types, suggesting a ‘push’ of undifferentiated, multipotent progenitors towards compensation for granule cell dearth. These data suggested that progenitors with the potential for multiple fates might differentiate towards repletion of deficient cell types, a possible developmental mechanism with therapeutic implications. Neural progenitors (donor or endogenous) might enable cell replacement in some developmental or degenerative diseases--most obviously in cases where a defect is intrinsic to the diseased cell, but also, under certain circumstances, when extrinsic pathologic forces may exist.

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Zelenova, Elena A., Nikolay V. Kondratyev, Tatyana V. Lezheiko, Grigoriy Y. Tsarapkin, Andrey I. Kryukov, Alexander E. Kishinevsky, Anna S. Tovmasyan, Ekaterina D. Momotyuk, Erdem B. Dashinimaev, and Vera E. Golimbet. "Characterisation of Neurospheres-Derived Cells from Human Olfactory Epithelium." Cells 10, no. 7 (July 4, 2021): 1690. http://dx.doi.org/10.3390/cells10071690.

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A major problem in psychiatric research is a deficit of relevant cell material of neuronal origin, especially in large quantities from living individuals. One of the promising options is cells from the olfactory neuroepithelium, which contains neuronal progenitors that ensure the regeneration of olfactory receptors. These cells are easy to obtain with nasal biopsies and it is possible to grow and cultivate them in vitro. In this work, we used RNAseq expression profiling and immunofluorescence microscopy to characterise neurospheres-derived cells (NDC), that simply and reliably grow from neurospheres (NS) obtained from nasal biopsies. We utilized differential expression analysis to explore the molecular changes that occur during transition from NS to NDC. We found that processes associated with neuronal and vascular cells are downregulated in NDC. A comparison with public transcriptomes revealed a depletion of neuronal and glial components in NDC. We also discovered that NDC have several metabolic features specific to neuronal progenitors treated with the fungicide maneb. Thus, while NDC retain some neuronal/glial identity, additional protocol alterations are needed to use NDC for mass sample collection in psychiatric research.

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Sheen, Volney L. "Periventricular Heterotopia: Shuttling of Proteins through Vesicles and Actin in Cortical Development and Disease." Scientifica 2012 (2012): 1–13. http://dx.doi.org/10.6064/2012/480129.

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During cortical development, proliferating neural progenitors exhibit polarized apical and basolateral membranes that are maintained by tightly controlled and membrane-specific vesicular trafficking pathways. Disruption of polarity through impaired delivery of proteins can alter cell fate decisions and consequent expansion of the progenitor pool, as well as impact the integrity of the neuroependymal lining. Loss of neuroependymal integrity disrupts radial glial scaffolding and alters initial neuronal migration from the ventricular zone. Vesicle trafficking is also required for maintenance of lipid and protein cycling within the leading and trailing edge of migratory neurons, as well as dendrites and synapses of mature neurons. Defects in this transport machinery disrupt neuronal identity, migration, and connectivity and give rise to a malformation of cortical development termed as periventricular heterotopia (PH). PH is characterized by a reduction in brain size, ectopic clusters of neurons localized along the lateral ventricle, and epilepsy and dyslexia. These anatomical anomalies correlate with developmental impairments in neural progenitor proliferation and specification, migration from loss of neuroependymal integrity and neuronal motility, and aberrant neuronal process extension. Genes causal for PH regulate vesicle-mediated endocytosis along an actin cytoskeletal network. This paper explores the role of these dynamic processes in cortical development and disease.

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Zaidi, Donia, Kaviya Chinnappa, and Fiona Francis. "Primary Cilia Influence Progenitor Function during Cortical Development." Cells 11, no. 18 (September 16, 2022): 2895. http://dx.doi.org/10.3390/cells11182895.

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Corticogenesis is an intricate process controlled temporally and spatially by many intrinsic and extrinsic factors. Alterations during this important process can lead to severe cortical malformations. Apical neuronal progenitors are essential cells able to self-amplify and also generate basal progenitors and/or neurons. Apical radial glia (aRG) are neuronal progenitors with a unique morphology. They have a long basal process acting as a support for neuronal migration to the cortical plate and a short apical process directed towards the ventricle from which protrudes a primary cilium. This antenna-like structure allows aRG to sense cues from the embryonic cerebrospinal fluid (eCSF) helping to maintain cell shape and to influence several key functions of aRG such as proliferation and differentiation. Centrosomes, major microtubule organising centres, are crucial for cilia formation. In this review, we focus on how primary cilia influence aRG function during cortical development and pathologies which may arise due to defects in this structure. Reporting and cataloguing a number of ciliary mutant models, we discuss the importance of primary cilia for aRG function and cortical development.

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Hatakeyama, Jun, and Kenji Shimamura. "The Pace of Neurogenesis Is Regulated by the Transient Retention of the Apical Endfeet of Differentiating Cells." Cerebral Cortex 29, no. 9 (October 11, 2018): 3725–37. http://dx.doi.org/10.1093/cercor/bhy252.

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Abstract The development of the mammalian cerebral cortex involves a variety of temporally organized events such as successive waves of neuronal production and the transition of progenitor competence for each neuronal subtype generated. The number of neurons generated in a certain time period, that is, the rate of neuron production, varies across the regions of the brain and the specific developmental stage; however, the underlying mechanism of this process is poorly understood. We have recently found that nascent neurons communicate with undifferentiated progenitors and thereby regulate neurogenesis, through a transiently retained apical endfoot that signals via the Notch pathway. Here, we report that the retention time length of the neuronal apical endfoot correlates with the rate of neuronal production in the developing mouse cerebral cortex. We further demonstrate that a forced reduction or extension of the retention period through the disruption or stabilization of adherens junction, respectively, resulted in the acceleration or deceleration of neurogenesis, respectively. Our results suggest that the apical endfeet of differentiating cells serve as a pace controller for neurogenesis, thereby assuring the well-proportioned laminar organization of the neocortex.

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Porat, Yael, Valentin Fulga, Danny Belkin, Svetlana Porozov, Yehudit Fisher, Michael Belkin, and Willam F. Silverman. "Adult Human Blood Leukocytes as an Efficient Source for Tissue-Committed Neural Progenitors." Blood 106, no. 11 (November 16, 2005): 1686. http://dx.doi.org/10.1182/blood.v106.11.1686.1686.

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Abstract In the last few years, significant progress has been made in the isolation and characterization of bone marrow stem cell populations and their potential to differentiate into a variety of cellular lineages. We hypothesized that peripheral blood can also be used as a source for precursor cells that can become committed progenitors for a variety of tissues. We report here the generation and characterization in vitro of neural progenitor cells from a newly discovered blood-derived multipotent cell population, named synergetic cell population (SCP). Human blood samples were obtained from the Israeli blood bank and SCP cells were purified based on cellular density. Neural progenitors were generated by culturing SCP cells in medium supplemented with autologous serum, followed by activation in a defined serum-free medium containing the specific differentiation-inducing factors F12, B27, bFGF, BDNF, and NGF. An average of 13.5x106 neural progenitor cells was generated from 450 ml blood. These cells developed irregular perikarya, from which filamentous extensions spread contacting neighboring cells and forming net-like structures. Immunostaining revealed that some of the cells express the early neuronal progenitor markers nestin and b-tubulin and Neu-N, a nuclear protein present in mature neurons. Other cells expressed glial-specific antigens, such as O4 (a marker of oligodendrocytes) and GFAP (a marker of astrocytes). Flow cytometry analysis showed that 44.4% and 34% of the cells were positive for nestin and b-tubulin, respectively. In addition to exhibiting phenotypic evidence of markers specific for the neural lineage, these progenitor cells also responded to the neurotransmitters glutamate and GABA, as detected by calcium influx through voltage-gated calcium channels, demonstrating functional differentiation. In this study we show that generation of neural progenitors from peripheral blood is feasible and efficient. Blood-derived angiogenic progenitors produced in our system are already safely and efficiently administrated to severe angina pectoris patients in a clinical trial we are conducting in Thailand (reported in a separate abstract by our group). The newly discovered source of these progenitors, the blood-derived multipotent population which we termed SCP, contains both hematopoietic stem cells as well as supportive cells that enable differentiation into various lineages. The therapeutic potential of these neural progenitors will be further characterized and evaluated in vivo using animal models.

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Gershon, A. A., J. Rudnick, L. Kalam, and K. Zimmerman. "The homeodomain-containing gene Xdbx inhibits neuronal differentiation in the developing embryo." Development 127, no. 13 (July 1, 2000): 2945–54. http://dx.doi.org/10.1242/dev.127.13.2945.

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The development of the vertebrate nervous system depends upon striking a balance between differentiating neurons and neural progenitors in the early embryo. Our findings suggest that the homeodomain-containing gene Xdbx regulates this balance by maintaining neural progenitor populations within specific regions of the neuroectoderm. In posterior regions of the Xenopus embryo, Xdbx is expressed in a bilaterally symmetric stripe that lies at the middle of the mediolateral axis of the neural plate. This stripe of Xdbx expression overlaps the expression domain of the proneural basic/helix-loop-helix-containing gene, Xash3, and is juxtaposed to the expression domains of Xenopus Neurogenin related 1 and N-tubulin, markers of early neurogenesis in the embryo. Xdbx overexpression inhibits neuronal differentiation in the embryo and when co-injected with Xash3, Xdbx inhibits the ability of Xash3 to induce ectopic neurogenesis. One role of Xdbx during normal development may therefore be to restrict spatially neuronal differentiation within the neural plate, possibly by altering the neuronal differentiation function of Xash3.

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Vanderluit, Jacqueline L., Crystal A. Wylie, Kelly A. McClellan, Noel Ghanem, Andre Fortin, Steve Callaghan, Jason G. MacLaurin, David S. Park, and Ruth S. Slack. "The Retinoblastoma family member p107 regulates the rate of progenitor commitment to a neuronal fate." Journal of Cell Biology 178, no. 1 (June 25, 2007): 129–39. http://dx.doi.org/10.1083/jcb.200703176.

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The Retinoblastoma protein p107 regulates the neural precursor pool in both the developing and adult brain. As p107-deficient mice exhibit enhanced levels of Hes1, we questioned whether p107 regulates neural precursor self-renewal through the repression of Hes1. p107 represses transcription at the Hes1 promoter. Despite an expanded neural precursor population, p107-null mice exhibit a striking reduction in the number of cortical neurons. Hes1 deficiency rescues neurosphere numbers in p107-null embryos. We find that the loss of a single Hes1 allele in vivo restores the number of neural precursor cells at the ventricular zone. Neuronal birthdating analysis reveals a dramatic reduction in the rate of neurogenesis, demonstrating impairment in p107−/− progenitors to commit to a neuronal fate. The loss of a single Hes1 allele restores the number of newly generated neurons in p107-deficient brains. Together, we identify a novel function for p107 in promoting neural progenitor commitment to a neuronal fate.

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Hui, Subhra Prakash, Tapas Chandra Nag, and Sukla Ghosh. "Neural cells and their progenitors in regenerating zebrafish spinal cord." International Journal of Developmental Biology 64, no. 4-5-6 (2020): 353–66. http://dx.doi.org/10.1387/ijdb.190130sg.

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The zebrafish (Danio rerio), among all amniotes is emerging as a powerful model to study vertebrate organogenesis and regeneration. In contrast to mammals, the adult zebrafish is capable of regenerating damaged axonal tracts; it can replace neurons and glia lost after spinal cord injury (SCI) and functionally recover. In the present paper, we report ultrastructural and cell biological analyses of regeneration processes after SCI. We have focused on event specific analyses of spinal cord regeneration involving different neuronal and glial cell progenitors, such as radial glia, oligodendrocyte progenitors (OPC), and Schwann cells. While comparing the different events, we frequently refer to previous ultrastructural analyses of central nervous system (CNS) injury in higher vertebrates. Our data show (a) the cellular events following injury, such as cell death and proliferation; (b) demyelination and remyelination followed by target innervation and regeneration of synaptic junctions and c) the existence of different progenitors and their roles during regeneration. The present ultrastructural analysis corroborates the cellular basis of regeneration in the zebrafish spinal cord and confirms the presence of both neuronal and different glial progenitors.

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Zeng, Chih-Wei. "Macrophage–Neuroglia Interactions in Promoting Neuronal Regeneration in Zebrafish." International Journal of Molecular Sciences 24, no. 7 (March 30, 2023): 6483. http://dx.doi.org/10.3390/ijms24076483.

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The human nervous system exhibits limited regenerative capabilities following damage to the central nervous system (CNS), leading to a scarcity of effective treatments for nerve function recovery. In contrast, zebrafish demonstrate remarkable regenerative abilities, making them an ideal model for studying the modulation of inflammatory processes after injury. Such research holds significant translational potential to enhance our understanding of recovery from damage and disease. Macrophages play a crucial role in tissue repair and regeneration, with their subpopulations indirectly promoting axonal regeneration through developmental signals. The AP-1 signaling pathway, mediated by TNF/Tnfrsf1a, can elevate HDAC1 expression and facilitate regeneration. Furthermore, following spinal cord injury (SCI), pMN progenitors have been observed to switch between oligodendrocyte and motor neuron fates, with macrophage-secreted TNF-α potentially regulating the differentiation of ependymal–radial glia progenitors and oligodendrocytes. Radial glial cells (RGs) are also essential for CNS regeneration in zebrafish, as they perform neurogenesis and gliogenesis, with specific RG subpopulations potentially existing for the generation of neurons and oligodendrocytes. This review article underscores the critical role of macrophages and their subpopulations in tissue repair and regeneration, focusing on their secretion of TNF-α, which promotes axonal regeneration in zebrafish. We also offer insights into the molecular mechanisms underlying TNF-α’s ability to facilitate axonal regeneration and explore the potential of pMN progenitor cells and RGs following SCI in zebrafish. The review concludes with a discussion of various unresolved questions in the field, and ideas are suggested for future research. Studying innate immune cell interactions with neuroglia following injury may lead to the development of novel strategies for treating the inflammatory processes associated with regenerative medicine, which are commonly observed in injury and disease.

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Yoshikawa, Gakushi, Toshihiko Momiyama, Soichi Oya, Keisuke Takai, Jun-ichi Tanaka, Shigeki Higashiyama, Nobuhito Saito, Takaaki Kirino, and Nobutaka Kawahara. "Induction of striatal neurogenesis and generation of region-specific functional mature neurons after ischemia by growth factors." Journal of Neurosurgery 113, no. 4 (October 2010): 835–50. http://dx.doi.org/10.3171/2010.2.jns09989.

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Object The capacity to replace lost neurons after insults is retained by several regions of adult mammalian brains. However, it is unknown how many neurons actually replace and mature into region-specific functional neurons to restore lost brain function. In this paper, the authors asked whether neuronal regeneration could be achieved efficaciously by growth factor treatment using a global ischemia model in rats, and they analyzed neuronal long-term maturation processes. Methods Rat global ischemia using a modified 4-vessel occlusion model was used to induce consistent ischemic neuronal injury in the dorsolateral striatum. To potentiate the proliferative response of neural progenitors, epidermal growth factor and fibroblast growth factor–2 were infused intraventricularly for 7 days from Day 2 after ischemia. Six weeks after ischemia, the number of neurons was counted in the defined dorsolateral striatum. To label the proliferating neural progenitors for tracing studies, 5-bromo-2′-deoxyuridine (BrdU; 150 mg/kg, twice a day) was injected intraperitoneally from Days 5 to 7, and immunohistochemical studies were conducted to explore the maturation of these progenitors. Migration of the progenitors was further studied by enhanced green fluorescent protein retrovirus injection. The effect of an antimitotic drug (cytosine arabinoside) on the neuronal count was also evaluated for contribution to regeneration. To see electrophysiological changes, treated rats were subjected to slice studies by whole-cell recordings. Finally, the effect of neural regeneration was assessed by motor performance by using the staircase test. Results Following epidermal growth factor and fibroblast growth factor–2 infusion into the lateral ventricles for 7 days beginning on Day 2, when severe neuronal loss in the adult striatum was confirmed (2.3% of normal controls), a significant increase of striatal neurons was observed at 6 weeks (~ 15% of normal controls) compared with vehicle controls (~ 5% of normal controls). Immunohistochemical studies by BrdU and enhanced green fluorescent protein retrovirus injection disclosed proliferation of neural progenitors in the subventricular zone and their migration to the ischemic striatum. By BrdU tracing study, NeuN- and BrdU-positive new neurons significantly increased at 6 and 12 weeks following the treatment. These accounted for 4.6 and 11.0% of the total neurons present, respectively. Antimitotic treatment demonstrated an approximately 66% reduction in neurons at 6 weeks. Further long-term studies showed dynamic changes of site-specific maturation among various neuronal subtypes even after 6 weeks. Electrophysiological properties of these newly appeared neurons underwent changes that conform to neonatal development. These regenerative changes were accompanied by a functional improvement of overall behavioral performance. Conclusions Treatment by growth factors significantly contributed to regeneration of mature striatal neurons after ischemia by endogenous neural progenitors, which was accompanied by electrophysiological maturation and improved motor performance. Recognition and improved understanding of these underlying dynamic processes will contribute to the development of novel and efficient regenerative therapies for brain injuries.

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Bertrand, Vincent, and Oliver Hobert. "Wnt asymmetry and the terminal division of neuronal progenitors." Cell Cycle 8, no. 13 (July 2009): 1973–78. http://dx.doi.org/10.4161/cc.8.13.9024.

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Luzzati, Federico, Silvia De Marchis, Aldo Fasolo, and Paolo Peretto. "Adult Neurogenesis and Local Neuronal Progenitors in the Striatum." Neurodegenerative Diseases 4, no. 4 (2007): 322–27. http://dx.doi.org/10.1159/000101889.

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Mazur-Kolecka, Bozena, Buddima Ranasinghe, and Janusz Frackowiak. "Influence of brain environment on proliferation of neuronal progenitors." Developmental Biology 306, no. 1 (June 2007): 392. http://dx.doi.org/10.1016/j.ydbio.2007.03.576.

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Fornasari, Benedetta Elena, Marwa El Soury, Silvia De Marchis, Isabelle Perroteau, Stefano Geuna, and Giovanna Gambarotta. "Neuregulin1 alpha activates migration of neuronal progenitors expressing ErbB4." Molecular and Cellular Neuroscience 77 (December 2016): 87–94. http://dx.doi.org/10.1016/j.mcn.2016.10.008.

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Munji, R. N., Y. Choe, G. Li, J. A. Siegenthaler, and S. J. Pleasure. "Wnt Signaling Regulates Neuronal Differentiation of Cortical Intermediate Progenitors." Journal of Neuroscience 31, no. 5 (February 2, 2011): 1676–87. http://dx.doi.org/10.1523/jneurosci.5404-10.2011.

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Zou, Qingjian, Quanmei Yan, Juan Zhong, Kepin Wang, Haitao Sun, Xiaoling Yi, and Liangxue Lai. "Direct Conversion of Human Fibroblasts into Neuronal Restricted Progenitors." Journal of Biological Chemistry 289, no. 8 (January 2, 2014): 5250–60. http://dx.doi.org/10.1074/jbc.m113.516112.

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Wiese, Carrie B., Nicole Fleming, Dennis P. Buehler, and E. Michelle Southard-Smith. "AUchl1-Histone2BmCherry:GFP-gpi BAC transgene for imaging neuronal progenitors." genesis 51, no. 12 (October 21, 2013): 852–61. http://dx.doi.org/10.1002/dvg.22716.

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Azzarelli, Roberta, Laura J. A. Hardwick, and Anna Philpott. "Emergence of neuronal diversity from patterning of telencephalic progenitors." Wiley Interdisciplinary Reviews: Developmental Biology 4, no. 3 (January 23, 2015): 197–214. http://dx.doi.org/10.1002/wdev.174.

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Moreno-Manzano, Victoria. "Ependymal cells in the spinal cord as neuronal progenitors." Current Opinion in Pharmacology 50 (February 2020): 82–87. http://dx.doi.org/10.1016/j.coph.2019.11.008.

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Kowalczyk, Tom, Adria Pontious, Chris Englund, Ray A. M. Daza, Francesco Bedogni, Rebecca Hodge, Alessio Attardo, Chris Bell, Wieland B. Huttner, and Robert F. Hevner. "Intermediate Neuronal Progenitors (Basal Progenitors) Produce Pyramidal–Projection Neurons for All Layers of Cerebral Cortex." Cerebral Cortex 19, no. 10 (January 23, 2009): 2439–50. http://dx.doi.org/10.1093/cercor/bhn260.

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Gonçalves, João Carlos, Tiago J. Dantas, and Richard B. Vallee. "Distinct roles for dynein light intermediate chains in neurogenesis, migration, and terminal somal translocation." Journal of Cell Biology 218, no. 3 (January 23, 2019): 808–19. http://dx.doi.org/10.1083/jcb.201806112.

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Cytoplasmic dynein participates in multiple aspects of neocortical development. These include neural progenitor proliferation, morphogenesis, and neuronal migration. The cytoplasmic dynein light intermediate chains (LICs) 1 and 2 are cargo-binding subunits, though their relative roles are not well understood. Here, we used in utero electroporation of shRNAs or LIC functional domains to determine the relative contributions of the two LICs in the developing rat brain. We find that LIC1, through BicD2, is required for apical nuclear migration in neural progenitors. In newborn neurons, we observe specific roles for LIC1 in the multipolar to bipolar transition and glial-guided neuronal migration. In contrast, LIC2 contributes to a novel dynein role in the little-studied mode of migration, terminal somal translocation. Together, our results provide novel insight into the LICs’ unique functions during brain development and dynein regulation overall.

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Morrow, Theresa, Mi-Ryoung Song, and Anirvan Ghosh. "Sequential specification of neurons and glia by developmentally regulated extracellular factors." Development 128, no. 18 (September 15, 2001): 3585–94. http://dx.doi.org/10.1242/dev.128.18.3585.

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Cortical progenitor cells give rise to neurons during embryonic development and to glia after birth. While lineage studies indicate that multipotent progenitor cells are capable of generating both neurons and glia, the role of extracellular signals in regulating the sequential differentiation of these cells is poorly understood. To investigate how factors in the developing cortex might influence cell fate, we developed a cortical slice overlay assay in which cortical progenitor cells are cultured over cortical slices from different developmental stages. We find that embryonic cortical progenitors cultured over embryonic cortical slices differentiate into neurons and those cultured over postnatal cortical slices differentiate into glia, suggesting that the fate of embryonic progenitors can be influenced by developmentally regulated signals. In contrast, postnatal progenitor cells differentiate into glial cells when cultured over either embryonic or postnatal cortical slices. Clonal analysis indicates that the postnatal cortex produces a diffusible factor that induces progenitor cells to adopt glial fates at the expense of neuronal fates. The effects of the postnatal cortical signals on glial cell differentiation are mimicked by FGF2 and CNTF, which induce glial fate specification and terminal glial differentiation respectively. These observations indicate that cell fate specification and terminal differentiation can be independently regulated and suggest that the sequential generation of neurons and glia in the cortex is regulated by a developmental increase in gliogenic signals.

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Muñoz, A., C. Wrighton, B. Seliger, J. Bernal, and H. Beug. "Thyroid hormone receptor/c-erbA: control of commitment and differentiation in the neuronal/chromaffin progenitor line PC12." Journal of Cell Biology 121, no. 2 (April 15, 1993): 423–38. http://dx.doi.org/10.1083/jcb.121.2.423.

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The c-erbA proto-oncogenes encode nuclear receptors for thyroid hormone (T3), a hormone intimately involved in mammalian brain maturation. To study thyroid hormone receptor (TR) action on neuronal cells in vitro, we expressed the chicken c-erbA/TR alpha-1 as well as its oncogenic variant v-erbA in the adrenal medulla progenitor cell line PC12. In the absence of T3, exogenous TR alpha-1 inhibits NGF-induced neuronal differentiation and represses neuron-specific gene expression. In contrast, TR alpha-1 allows normal differentiation and neuronal gene expression to occur in the presence of T3. Finally, TR alpha-1-expressing cells become NGF-responsive for proliferation when T3 is absent, but NGF-dependent for survival in presence of T3. A similar differentiation induction by NGF plus T3 was observed in a central nervous system-derived neuronal cell line (E 18) expressing exogenous TR alpha-1. Together with the finding that TR alpha-1 constitutively blocked dexamethasone-induced differentiation of PC12 cells into the chromaffin pathway, these results suggest that TR alpha-1 plays an important role in regulating commitment and maturation of neuronal progenitors. In contrast, the v-erbA oncogene, a mutated, oncogenic version of TR alpha-1, partially but constitutively inhibited NGF-induced neuronal differentiation of PC12 cells and potentiated dexamethasone-induced chromaffin differentiation, giving rise to an aberrant "interlineage" cell phenotype.

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Puch, S., S. Armeanu, C. Kibler, K. R. Johnson, C. A. Muller, M. J. Wheelock, and G. Klein. "N-cadherin is developmentally regulated and functionally involved in early hematopoietic cell differentiation." Journal of Cell Science 114, no. 8 (April 15, 2001): 1567–77. http://dx.doi.org/10.1242/jcs.114.8.1567.

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The cadherins, an important family of cell adhesion molecules, are known to play major roles during embryonic development and in the maintenance of solid tissue architecture. In the hematopoietic system, however, little is known of the role of this cell adhesion family. By RT-PCR, western blot analysis and immunofluorescence staining we show that N-cadherin, a classical type I cadherin mainly expressed on neuronal, endothelial and muscle cells, is expressed on the cell surface of resident bone marrow stromal cells. FACS analysis of bone marrow mononuclear cells revealed that N-cadherin is also expressed on a subpopulation of early hematopoietic progenitor cells. Triple-color FACS analysis defined a new CD34(+) CD19(+) N-cadherin(+) progenitor cell population. During further differentiation, however, N-cadherin expression is lost. Treatment of CD34(+) progenitor cells with function-perturbing N-cadherin antibodies drastically diminished colony formation, indicating a direct involvement of N-cadherin in the differentiation program of early hematopoietic progenitors. N-cadherin can also mediate adhesive interactions within the bone marrow as demonstrated by inhibition of homotypic interactions of bone-marrow-derived cells with N-cadherin antibodies. Together, these data strongly suggest that N-cadherin is involved in the development and retention of early hematopoietic progenitors within the bone marrow microenvironment.

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Paris, Maryline, Wen-Horng Wang, Min-Hwa Shin, David S. Franklin, and Ourania M. Andrisani. "Homeodomain Transcription Factor Phox2a, via Cyclic AMP-Mediated Activation, Induces p27Kip1 Transcription, Coordinating Neural Progenitor Cell Cycle Exit and Differentiation." Molecular and Cellular Biology 26, no. 23 (September 18, 2006): 8826–39. http://dx.doi.org/10.1128/mcb.00575-06.

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ABSTRACT Mechanisms coordinating neural progenitor cell cycle exit and differentiation are incompletely understood. The cyclin-dependent kinase inhibitor p27Kip1 is transcriptionally induced, switching specific neural progenitors from proliferation to differentiation. However, neuronal differentiation-specific transcription factors mediating p27Kip1 transcription have not been identified. We demonstrate the homeodomain transcription factor Phox2a, required for central nervous system (CNS)- and neural crest (NC)-derived noradrenergic neuron differentiation, coordinates cell cycle exit and differentiation by inducing p27Kip1 transcription. Phox2a transcription and activation in the CNS-derived CAD cell line and primary NC cells is mediated by combined cyclic AMP (cAMP) and bone morphogenetic protein 2 (BMP2) signaling. In the CAD cellular model, cAMP and BMP2 signaling initially induces proliferation of the undifferentiated precursors, followed by p27Kip1 transcription, G1 arrest, and neuronal differentiation. Small interfering RNA silencing of either Phox2a or p27Kip1 suppresses p27Kip1 transcription and neuronal differentiation, suggesting a causal link between p27Kip1 expression and differentiation. Conversely, ectopic Phox2a expression via the Tet-off expression system promotes accelerated CAD cell neuronal differentiation and p27Kip1 transcription only in the presence of cAMP signaling. Importantly, endogenous or ectopically expressed Phox2a activated by cAMP signaling binds homeodomain cis-acting elements of the p27Kip1 promoter in vivo and mediates p27Kip1-luciferase expression in CAD and NC cells. We conclude that developmental cues of cAMP signaling causally link Phox2a activation with p27Kip1 transcription, thereby coordinating neural progenitor cell cycle exit and differentiation.

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Kim, Dong Kyu, Hyobin Jeong, Jingi Bae, Moon-Yong Cha, Moonkyung Kang, Dongjin Shin, Shinwon Ha, et al. "Aβ-induced mitochondrial dysfunction in neural progenitors controls KDM5A to influence neuronal differentiation." Experimental & Molecular Medicine, September 2, 2022. http://dx.doi.org/10.1038/s12276-022-00841-w.

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AbstractMitochondria in neural progenitors play a crucial role in adult hippocampal neurogenesis by being involved in fate decisions for differentiation. However, the molecular mechanisms by which mitochondria are related to the genetic regulation of neuronal differentiation in neural progenitors are poorly understood. Here, we show that mitochondrial dysfunction induced by amyloid-beta (Aβ) in neural progenitors inhibits neuronal differentiation but has no effect on the neural progenitor stage. In line with the phenotypes shown in Alzheimer’s disease (AD) model mice, Aβ-induced mitochondrial damage in neural progenitors results in deficits in adult hippocampal neurogenesis and cognitive function. Based on hippocampal proteome changes after mitochondrial damage in neural progenitors identified through proteomic analysis, we found that lysine demethylase 5A (KDM5A) in neural progenitors epigenetically suppresses differentiation in response to mitochondrial damage. Mitochondrial damage characteristically causes KDM5A degradation in neural progenitors. Since KDM5A also binds to and activates neuronal genes involved in the early stage of differentiation, functional inhibition of KDM5A consequently inhibits adult hippocampal neurogenesis. We suggest that mitochondria in neural progenitors serve as the checkpoint for neuronal differentiation via KDM5A. Our findings not only reveal a cell-type-specific role of mitochondria but also suggest a new role of KDM5A in neural progenitors as a mediator of retrograde signaling from mitochondria to the nucleus, reflecting the mitochondrial status.

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Journal articles on the topic 'Neuronal progenitors'

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