Journal articles: 'Neurogenesis; ubiquitin; embryonic stem cell'

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Guan, Kaomei, Hong Chang, Alexandra Rolletschek, and Anna M. Wobus. "Embryonic stem cell-derived neurogenesis." Cell and Tissue Research 305, no. 2 (June 6, 2001): 171–76. http://dx.doi.org/10.1007/s004410100416.

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Germain, Noélle, Erin Banda, and Laura Grabel. "Embryonic stem cell neurogenesis and neural specification." Journal of Cellular Biochemistry 111, no. 3 (June 29, 2010): 535–42. http://dx.doi.org/10.1002/jcb.22747.

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Krichevsky, Anna M., Kai-C. Sonntag, Ole Isacson, and Kenneth S. Kosik. "Specific MicroRNAs Modulate Embryonic Stem Cell-Derived Neurogenesis." STEM CELLS 24, no. 4 (April 2006): 857–64. http://dx.doi.org/10.1634/stemcells.2005-0441.

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Zhang, Juan, and Jianwei Jiao. "Molecular Biomarkers for Embryonic and Adult Neural Stem Cell and Neurogenesis." BioMed Research International 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/727542.

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The procedure of neurogenesis has made numerous achievements in the past decades, during which various molecular biomarkers have been emerging and have been broadly utilized for the investigation of embryonic and adult neural stem cell (NSC). Nevertheless, there is not a consistent and systematic illustration to depict the functional characteristics of the specific markers expressed in distinct cell types during the different stages of neurogenesis. Here we gathered and generalized a series of NSC biomarkers emerging during the procedures of embryonic and adult neural stem cell, which may be used to identify the subpopulation cells with distinguishing characters in different timeframes of neurogenesis. The identifications of cell patterns will provide applications to the detailed investigations of diverse developmental cell stages and the extents of cell differentiation, which will facilitate the tracing of cell time-course and fate determination of specific cell types and promote the further and literal discoveries of embryonic and adult neurogenesis. Meanwhile, via the utilization of comprehensive applications under the aiding of the systematic knowledge framework, researchers may broaden their insights into the derivation and establishment of novel technologies to analyze the more detailed process of embryogenesis and adult neurogenesis.

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Amura, Claudia R., Lindsay Marek, Robert A. Winn, and Lynn E. Heasley. "Inhibited Neurogenesis in JNK1-Deficient Embryonic Stem Cells." Molecular and Cellular Biology 25, no. 24 (December 15, 2005): 10791–802. http://dx.doi.org/10.1128/mcb.25.24.10791-10802.2005.

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ABSTRACT The JNKs are components of stress signaling pathways but also regulate morphogenesis and differentiation. Previously, we invoked a role for the JNKs in nerve growth factor (NGF)-stimulated PC12 cell neural differentiation (L. Marek et al., J. Cell. Physiol. 201:459-469, 2004; E. Zentrich et al., J. Biol. Chem. 277:4110-4118, 2002). Herein, the role for JNKs in neural differentiation and transcriptional regulation of the marker gene, NFLC, modeled in mouse embryonic stem (ES) cells was studied. NFLC-luciferase reporters revealed the requirement for NFLC promoter sequences encompassing base pairs −128 to −98 relative to the transcriptional start site as well as a proximal cyclic AMP response element-activating transcription factor binding site at −45 to −38 base pairs for transcriptional induction in NGF-treated PC12 cells and neurally differentiated ES cells. The findings reveal common promoter sequences that integrate conserved signal pathways in both PC12 cell and ES cell systems. To test the requirement for the JNK pathway in ES cell neurogenesis, ES cell lines bearing homozygous disruptions of the jnk1, jnk2, or jnk3 genes were derived and submitted to an embryoid body (EB) differentiation protocol. Neural differentiation was observed in wild-type, JNK2−/−, and JNK3−/− cultures but not in JNK1−/− EBs. Rather, an outgrowth of cells with epithelial morphology and enhanced E-cadherin expression but low NFLC mRNA and protein was observed in JNK1−/− cultures. The expression of wnt-4 and wnt-6, identified inhibitors of ES cell neurogenesis, was significantly elevated in JNK1−/− cultures relative to wild-type, JNK2−/−, and JNK3−/− cultures. Moreover, the Wnt antagonist, sFRP-2, partially rescued neural differentiation in JNK1−/− cultures. Thus, a genetic approach using JNK-deficient ES cells reveals a novel role for JNK1 involving repression of Wnt expression in neural differentiation modeled in murine ES cells.

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Banda, Erin, Anna McKinsey, Noelle Germain, James Carter, Nickesha Camille Anderson, and Laura Grabel. "Cell Polarity and Neurogenesis in Embryonic Stem Cell-Derived Neural Rosettes." Stem Cells and Development 24, no. 8 (April 15, 2015): 1022–33. http://dx.doi.org/10.1089/scd.2014.0415.

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Gotoh, Yukiko. "IL2 Neural stem cell regulation and brain development." Neuro-Oncology Advances 3, Supplement_6 (December 1, 2021): vi1. http://dx.doi.org/10.1093/noajnl/vdab159.001.

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Abstract Quiescent neural stem cells (NSCs) in the adult mouse brain are the source of neurogenesis that regulates innate and adaptive behaviors. Adult NSCs in the subventricular zone (SVZ) are derived from a subpopulation of embryonic neural stem-progenitor cells (NPCs) that is characterized by a slower cell cycle relative to the more abundant rapid cycling NPCs that build the brain. We have previously shown that slow cell cycle can cause the establishment of adult NSCs at the SVZ, although the underlying mechanism remains unknown. We found that Notch and an effector Hey1 form a module that is upregulated by cell cycle arrest in slowly dividing NPCs. In contrast to the oscillatory expression of the Notch effectors Hes1 and Hes5 in fast cycling progenitors, Hey1 displays a non-oscillatory stationary expression pattern and contributes to the long-term maintenance of NSCs. These findings reveal a novel division of labor in Notch effectors where cell cycle rate biases effector selection and cell fate. I will also discuss the heterogeneity of slowly dividing embryonic NPCs and the lineage relationship between adult NSCs and ependymal cells, which together form the niche for adult neurogenesis at the SVZ.

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Wang, Dian, Fan Bu, and Weiwei Zhang. "The Role of Ubiquitination in Regulating Embryonic Stem Cell Maintenance and Cancer Development." International Journal of Molecular Sciences 20, no. 11 (May 30, 2019): 2667. http://dx.doi.org/10.3390/ijms20112667.

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Ubiquitination regulates nearly every aspect of cellular events in eukaryotes. It modifies intracellular proteins with 76-amino acid polypeptide ubiquitin (Ub) and destines them for proteolysis or activity alteration. Ubiquitination is generally achieved by a tri-enzyme machinery involving ubiquitin activating enzymes (E1), ubiquitin conjugating enzymes (E2) and ubiquitin ligases (E3). E1 activates Ub and transfers it to the active cysteine site of E2 via a transesterification reaction. E3 coordinates with E2 to mediate isopeptide bond formation between Ub and substrate protein. The E1-E2-E3 cascade can create diverse types of Ub modifications, hence effecting distinct outcomes on the substrate proteins. Dysregulation of ubiquitination results in severe consequences and human diseases. There include cancers, developmental defects and immune disorders. In this review, we provide an overview of the ubiquitination machinery and discuss the recent progresses in the ubiquitination-mediated regulation of embryonic stem cell maintenance and cancer biology.

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Guerra, Gabriela Maria, Doreen May, Torsten Kroll, Philipp Koch, Marco Groth, Zhao-Qi Wang, Tang-Liang Li, and Paulius Grigaravičius. "Cell Type-Specific Role of RNA Nuclease SMG6 in Neurogenesis." Cells 10, no. 12 (November 30, 2021): 3365. http://dx.doi.org/10.3390/cells10123365.

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SMG6 is an endonuclease, which cleaves mRNAs during nonsense-mediated mRNA decay (NMD), thereby regulating gene expression and controling mRNA quality. SMG6 has been shown as a differentiation license factor of totipotent embryonic stem cells. To investigate whether it controls the differentiation of lineage-specific pluripotent progenitor cells, we inactivated Smg6 in murine embryonic neural stem cells. Nestin-Cre-mediated deletion of Smg6 in mouse neuroprogenitor cells (NPCs) caused perinatal lethality. Mutant mice brains showed normal structure at E14.5 but great reduction of the cortical NPCs and late-born cortical neurons during later stages of neurogenesis (i.e., E18.5). Smg6 inactivation led to dramatic cell death in ganglionic eminence (GE) and a reduction of interneurons at E14.5. Interestingly, neurosphere assays showed self-renewal defects specifically in interneuron progenitors but not in cortical NPCs. RT-qPCR analysis revealed that the interneuron differentiation regulators Dlx1 and Dlx2 were reduced after Smg6 deletion. Intriguingly, when Smg6 was deleted specifically in cortical and hippocampal progenitors, the mutant mice were viable and showed normal size and architecture of the cortex at E18.5. Thus, SMG6 regulates cell fate in a cell type-specific manner and is more important for neuroprogenitors originating from the GE than for progenitors from the cortex.

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Li, Hui, Zhihong Zhang, Beibei Wang, Junmei Zhang, Yingming Zhao, and Ying Jin. "Wwp2-Mediated Ubiquitination of the RNA Polymerase II Large Subunit in Mouse Embryonic Pluripotent Stem Cells." Molecular and Cellular Biology 27, no. 15 (May 25, 2007): 5296–305. http://dx.doi.org/10.1128/mcb.01667-06.

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ABSTRACT Ubiquitination and the degradation of the large subunit of RNA polymerase II, Rpb1, is not only involved in DNA damage-induced arrest but also in other transcription-obstructing events. However, the ubiquitin ligases responsible for DNA damage-independent processes in mammalian cells remain to be identified. Here, we identified Wwp2, a mouse HECT domain ubiquitin E3 ligase, as a novel ubiquitin ligase of Rpb1. We found that Wwp2 specifically interacted with mouse Rpb1 and targeted it for ubiquitination both in vitro and in vivo. Interestingly, the interaction with and ubiquitination of Rpb1 was dependent neither on its phosphorylation state nor on DNA damage. However, the enzymatic activity of Wwp2 was absolutely required for its ubiquitin modification of Rpb1. Furthermore, our study indicates that the interaction between Wwp2 and Rpb1 was mediated through WW domain of Wwp2 and C-terminal domain of Rpb1, respectively. Strikingly, downregulation of Wwp2 expression compromised Rpb1 ubiquitination and elevated its intracellular steady-state protein level significantly. Importantly, we identified six lysine residues in the C-terminal domain of Rpb1 as ubiquitin acceptor sites mediated by Wwp2. These results indicate that Wwp2 plays an important role in regulating expression of Rpb1 in normal physiological conditions.

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Skopalová, Kateřina, Katarzyna Anna Radaszkiewicz, Věra Kašpárková, Jaroslav Stejskal, Patrycja Bober, Ita Junkar, Miran Mozetič, et al. "Modulation of Differentiation of Embryonic Stem Cells by Polypyrrole: The Impact on Neurogenesis." International Journal of Molecular Sciences 22, no. 2 (January 6, 2021): 501. http://dx.doi.org/10.3390/ijms22020501.

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The active role of biomaterials in the regeneration of tissues and their ability to modulate the behavior of stem cells in terms of their differentiation is highly advantageous. Here, polypyrrole, as a representantive of electro-conducting materials, is found to modulate the behavior of embryonic stem cells. Concretely, the aqueous extracts of polypyrrole induce neurogenesis within embryonic bodies formed from embryonic stem cells. This finding ledto an effort to determine the physiological cascade which is responsible for this effect. The polypyrrole modulates signaling pathways of Akt and ERK kinase through their phosphorylation. These effects are related to the presence of low-molecular-weight compounds present in aqueous polypyrrole extracts, determined by mass spectroscopy. The results show that consequences related to the modulation of stem cell differentiation must also be taken into account when polypyrrole is considered as a biomaterial.

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Cai, Chunyu, Jeffrey Thorne, and Laura Grabel. "Hedgehog Serves as a Mitogen and Survival Factor During Embryonic Stem Cell Neurogenesis." Stem Cells 26, no. 5 (May 2008): 1097–108. http://dx.doi.org/10.1634/stemcells.2007-0684.

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Okano, Hideyuki, and Kazunobu Sawamoto. "Neural stem cells: involvement in adult neurogenesis and CNS repair." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1500 (March 13, 2008): 2111–22. http://dx.doi.org/10.1098/rstb.2008.2264.

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Recent advances in stem cell research, including the selective expansion of neural stem cells (NSCs) in vitro , the induction of particular neural cells from embryonic stem cells in vitro , the identification of NSCs or NSC-like cells in the adult brain and the detection of neurogenesis in the adult brain (adult neurogenesis), have laid the groundwork for the development of novel therapies aimed at inducing regeneration in the damaged central nervous system (CNS). There are two major strategies for inducing regeneration in the damaged CNS: (i) activation of the endogenous regenerative capacity and (ii) cell transplantation therapy. In this review, we summarize the recent findings from our group and others on NSCs, with respect to their role in insult-induced neurogenesis (activation of adult NSCs, proliferation of transit-amplifying cells, migration of neuroblasts and survival and maturation of the newborn neurons), and implications for therapeutic interventions, together with tactics for using cell transplantation therapy to treat the damaged CNS.

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Morgun, A. V., E. D. Osipova, E. B. Boytsova, A. N. Shuvaev, Yu K. Komleva, L. V. Trufanova, E. F. Vais, and A. B. Salmina. "Astroglia-mediated regulation of cell development in the model of neurogenic niche in vitro treated with Aβ1-42." Biomeditsinskaya Khimiya 65, no. 5 (2019): 366–73. http://dx.doi.org/10.18097/pbmc20196505366.

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Neurogenesis is a complex process which governs embryonic brain development and is importants for brain plasticity throughout the whole life. Postnatal neurogenesis occurs in neurogenic niches that regulate the processes of proliferation and differentiation of stem and progenitor cells under the action of stimuli that trigger the mechanisms of neuroplasticity. Cells of glial and endothelial origin are the key regulators of neurogenesis. It is known that physiological neurogeneses is crucial for memory formation, whereas reparative neurogenesis provides partial repair of altered brain structure and compensation of neurological deficits caused by brain injury. Dysregulation of neurogenesis is a characteristics of various neurodevelopmental and neurodegenerative diseases, particularly, Alzheimer's disease which is very important medical and social problem. In the in vitro model of the neurogenic niche using hippocampal neurospheres as a source of stem/progenitor cells and astrocytes, we studied effects of astrocyte activation on the expression of markers of different stages of cell proliferation and differentiation. We found that aberrant mechanisms of development of stem and progenitor cells, caused by the beta-amyloid (Aβ1-42), can be partially restored by targeted activation of GFAP-expressing cells in the neurogenic niche.

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Gil, Jung-Eun, Dong-Hun Woo, Joong-Hyun Shim, Sung-Eun Kim, Hyun-Ju You, Sung-Hye Park, Sun Ha Paek, Suel-Kee Kim, and Jong-Hoon Kim. "Vitronectin promotes oligodendrocyte differentiation during neurogenesis of human embryonic stem cells." FEBS Letters 583, no. 3 (January 20, 2009): 561–67. http://dx.doi.org/10.1016/j.febslet.2008.12.061.

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Tata, Mathew, Ivan Wall, Andy Joyce, Joaquim M. Vieira, Nicoletta Kessaris, and Christiana Ruhrberg. "Regulation of embryonic neurogenesis by germinal zone vasculature." Proceedings of the National Academy of Sciences 113, no. 47 (November 7, 2016): 13414–19. http://dx.doi.org/10.1073/pnas.1613113113.

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In the adult rodent brain, new neurons are born in two germinal regions that are associated with blood vessels, and blood vessels and vessel-derived factors are thought to regulate the activity of adult neural stem cells. Recently, it has been proposed that a vascular niche also regulates prenatal neurogenesis. Here we identify the mouse embryo hindbrain as a powerful model to study embryonic neurogenesis and define the relationship between neural progenitor cell (NPC) behavior and vessel growth. Using this model, we show that a subventricular vascular plexus (SVP) extends through a hindbrain germinal zone populated by NPCs whose peak mitotic activity follows a surge in SVP growth. Hindbrains genetically defective in SVP formation owing to constitutive NRP1 loss showed a premature decline in both NPC activity and hindbrain growth downstream of precocious cell cycle exit, premature neuronal differentiation, and abnormal mitosis patterns. Defective regulation of NPC activity was not observed in mice lacking NRP1 expression by NPCs, but instead in mice lacking NRP1 selectively in endothelial cells, yet was independent of vascular roles in hindbrain oxygenation. Therefore, germinal zone vascularization sustains NPC proliferation in the prenatal brain.

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Ramasamy, Saravana Kumar, and Nibedita Lenka. "Notch Exhibits Ligand Bias and Maneuvers Stage-Specific Steering of Neural Differentiation in Embryonic Stem Cells." Molecular and Cellular Biology 30, no. 8 (February 12, 2010): 1946–57. http://dx.doi.org/10.1128/mcb.01419-09.

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ABSTRACT Notch dictates multiple developmental events, including stem cell maintenance and differentiation, through intercellular communication. However, its temporal influence during early development and, of particular interest, its regulation of binary fate decision at different stages during neurogenesis are among the least explored. Here, using an embryonic stem cell (ESC) model, we have deciphered Notch ligand preference during ESC commitment to different germ layers and determined the stage-specific temporal effect of Notch during neural differentiation. ESCs during maintenance remain impervious to Notch inhibition. However, Notch activation promotes differentiation even in the presence of leukemia inhibitory factor (LIF), displaying ligand preference-associated lineage discrimination, where Jagged-1 favors neural commitment and Delta-like-4 favors the mesoderm. This differential ligand action involves a combination of Notch receptors influencing specific downstream target gene expression. Though Notch activation during early neural differentiation specifically promotes neural stem cells or early neural progenitors and delays their maturation, its inhibition promotes late neural progenitors and expedites neurogenesis, with a preference for neurons over glia. However, gliogenesis is promoted upon Notch activation only when executed in combination with ciliary neurotrophic factor. Thus, our investigation underscores a multifaceted role of Notch, demonstrating the interdependency of ligand usage and lineage specification and Notch acting as a master switch, displaying stage-specific influence on neurogenesis.

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Hao, Lei, Zhongmin Zou, Hong Tian, Yubo Zhang, Huchuan Zhou, and Lei Liu. "Stem Cell-Based Therapies for Ischemic Stroke." BioMed Research International 2014 (2014): 1–17. http://dx.doi.org/10.1155/2014/468748.

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In recent years, stem cell-based approaches have attracted more attention from scientists and clinicians due to their possible therapeutical effect on stroke. Animal studies have demonstrated that the beneficial effects of stem cells including embryonic stem cells (ESCs), inducible pluripotent stem cells (iPSCs), neural stem cells (NSCs), and mesenchymal stem cell (MSCs) might be due to cell replacement, neuroprotection, endogenous neurogenesis, angiogenesis, and modulation on inflammation and immune response. Although several clinical studies have shown the high efficiency and safety of stem cell in stroke management, mainly MSCs, some issues regarding to cell homing, survival, tracking, safety, and optimal cell transplantation protocol, such as cell dose and time window, should be addressed. Undoubtably, stem cell-based gene therapy represents a novel potential therapeutic strategy for stroke in future.

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Seong, Kyung-Joo, Seungho Choi, Hyun-Gwan Lee, Joon Haeng Rhee, Jin Ho Lee, Jeong-Tae Koh, Sun-Hun Kim, Won-Seok Choi, Ji-Yeon Jung, and Won-Jae Kim. "Toll-Like Receptor 5 Promotes the Neurogenesis From Embryonic Stem Cells and Adult Hippocampal Neural Stem Cells in Mice." Stem Cells 40, no. 3 (February 20, 2022): 303–17. http://dx.doi.org/10.1093/stmcls/sxab025.

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Abstract Toll-like receptors (TLRs) make a crucial contribution to the innate immune response. TLR5 was expressed in embryoid body derived from mouse embryonic stem cells (mESCs) and βIII-tubulin-positive cells under all-trans retinoic acid-treated condition. TLR5 was upregulated during neural differentiation from mESCs and augmented the neural differentiation of mESCs via nuclear factor-κB and interleukin 6/CREB pathways. Besides, TLR5 was expressed in SOX2- or doublecortin-positive cells in the subgranular zone of the hippocampal dentate gyrus where adult neurogenesis occurs. TLR5 inhibited the proliferation of adult hippocampal neural stem cells (NSCs) by regulating the cell cycle and facilitated the neural differentiation from the adult hippocampal NSCs via JNK pathway. Also, TLR5 deficiency impaired fear memory performance in mice. Our data suggest that TLR5 is a crucial modulator of neurogenesis from mESCs and adult hippocampal NSCs in mice and represents a new therapeutic target in neurological disorders related to cognitive function.

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Lokapally, Ashwin, Herbert Neuhaus, Juliane Herfurth, and Thomas Hollemann. "Interplay of TRIM2 E3 Ubiquitin Ligase and ALIX/ESCRT Complex: Control of Developmental Plasticity During Early Neurogenesis." Cells 9, no. 7 (July 20, 2020): 1734. http://dx.doi.org/10.3390/cells9071734.

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Tripartite motif 2 (TRIM2) drives neurite outgrowth and polarization, is involved in axon specification, and confers neuroprotective functions during rapid ischemia. The mechanisms controlling neuronal cell fate determination and differentiation are fundamental for neural development. Here, we show that in Xenopus, trim2 knockdown affects primary neurogenesis and neural progenitor cell survival. Embryos also suffer from severe craniofacial malformation, a reduction in brain volume, and the loss of motor sensory function. Using a high-throughput LC-MS/MS approach with GST-Trim2 as bait, we pulled down ALG-2 interacting protein X (Alix) from Xenopus embryonic lysates. We demonstrate that the expression of trim2/TRIM2 and alix/ALIX overlap during larval development and on a cellular level in cell culture. Interestingly, trim2 morphants showed a clustering and apoptosis of neural progenitors, which are phenotypic hallmarks that are also observed in Alix KO mice. Therefore, we propose that the interaction of Alix and Trim2 plays a key role in the determination and differentiation of neural progenitors via the modulation of cell proliferation/apoptosis during neurogenesis.

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Ji, Fen, Tianjin Shen, Wenzheng Zou, and Jianwei Jiao. "UCP2 Regulates Embryonic Neurogenesis via ROS-Mediated Yap Alternation in the Developing Neocortex." STEM CELLS 35, no. 6 (March 27, 2017): 1479–92. http://dx.doi.org/10.1002/stem.2605.

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Mora-Bermúdez, Felipe, and Wieland B. Huttner. "Novel insights into mammalian embryonic neural stem cell division: focus on microtubules." Molecular Biology of the Cell 26, no. 24 (December 2015): 4302–6. http://dx.doi.org/10.1091/mbc.e15-03-0152.

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During stem cell divisions, mitotic microtubules do more than just segregate the chromosomes. They also determine whether a cell divides virtually symmetrically or asymmetrically by establishing spindle orientation and the plane of cell division. This can be decisive for the fate of the stem cell progeny. Spindle defects have been linked to neurodevelopmental disorders, yet the role of spindle orientation for mammalian neurogenesis has remained controversial. Here we explore recent advances in understanding how the microtubule cytoskeleton influences mammalian neural stem cell division. Our focus is primarily on the role of spindle microtubules in the development of the cerebral cortex. We also highlight unique characteristics in the architecture and dynamics of cortical stem cells that are tightly linked to their mode of division. These features contribute to setting these cells apart as mitotic “rule breakers,” control how asymmetric a division is, and, we argue, are sufficient to determine the fate of the neural stem cell progeny in mammals.

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Šafaříková, Eva, Jiří Ehlich, Stanislav Stříteský, Martin Vala, Martin Weiter, Jiří Pacherník, Lukáš Kubala, and Jan Víteček. "Conductive Polymer PEDOT:PSS-Based Platform for Embryonic Stem-Cell Differentiation." International Journal of Molecular Sciences 23, no. 3 (January 20, 2022): 1107. http://dx.doi.org/10.3390/ijms23031107.

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Organic semiconductors are constantly gaining interest in regenerative medicine. Their tunable physico-chemical properties, including electrical conductivity, are very promising for the control of stem-cell differentiation. However, their use for combined material-based and electrical stimulation remains largely underexplored. Therefore, we carried out a study on whether a platform based on the conductive polymer poly(3,4-ethylenedioxythiophene):polystyrene sulfonate (PEDOT:PSS) can be beneficial to the differentiation of mouse embryonic stem cells (mESCs). The platform was prepared using the layout of a standard 24-well cell-culture plate. Polyethylene naphthalate foil served as the substrate for the preparation of interdigitated gold electrodes by physical vapor deposition. The PEDOT:PSS pattern was fabricated by precise screen printing over the gold electrodes. The PEDOT:PSS platform was able to produce higher electrical current with the pulsed-direct-current (DC) electrostimulation mode (1 Hz, 200 mV/mm, 100 ms pulse duration) compared to plain gold electrodes. There was a dominant capacitive component. In proof-of-concept experiments, mESCs were able to respond to such electrostimulation by membrane depolarization and elevation of cytosolic calcium. Further, the PEDOT:PSS platform was able to upregulate cardiomyogenesis and potentially inhibit early neurogenesis per se with minor contribution of electrostimulation. Hence, the present work highlights the large potential of PEDOT:PSS in regenerative medicine.

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Chen, Ching-Wen, Chin-San Liu, Ing-Ming Chiu, Shih-Cheng Shen, Hung-Chuan Pan, Kun-Hsiung Lee, Shinn-Zong Lin, and Hong-Lin Su. "The signals of FGFs on the neurogenesis of embryonic stem cells." Journal of Biomedical Science 17, no. 1 (2010): 33. http://dx.doi.org/10.1186/1423-0127-17-33.

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Hubbard, Kyle S., Ian M. Gut, Megan E. Lyman, and Patrick M. McNutt. "Longitudinal RNA sequencing of the deep transcriptome during neurogenesis of cortical glutamatergic neurons from murine ESCs." F1000Research 2 (February 7, 2013): 35. http://dx.doi.org/10.12688/f1000research.2-35.v1.

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Using paired-end RNA sequencing, we have quantified the deep transcriptional changes that occur during differentiation of murine embryonic stem cells into a highly enriched population of glutamatergic cortical neurons. These data provide a detailed and nuanced account of longitudinal changes in the transcriptome during neurogenesis and neuronal maturation, starting from mouse embryonic stem cells and progressing through neuroepithelial stem cell induction, radial glial cell formation, neurogenesis, neuronal maturation and cortical patterning. Understanding the transcriptional mechanisms underlying the differentiation of stem cells into mature, glutamatergic neurons of cortical identity has myriad applications, including the elucidation of mechanisms of cortical patterning; identification of neurogenic processes; modeling of disease states; detailing of the host cell response to neurotoxic stimuli; and determination of potential therapeutic targets. In future work we anticipate correlating changes in longitudinal gene expression to other cell parameters, including neuronal function as well as characterizations of the proteome and metabolome. In this data article, we describe the methods used to produce the data and present the raw sequence read data in FASTQ files, sequencing run statistics and a summary flatfile of raw counts for 22,164 genes across 31 samples, representing 3-5 biological replicates at each timepoint. We propose that this data will be a valuable contribution to diverse research efforts in bioinformatics, stem cell research and developmental neuroscience studies.

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Telias, Michael, Menahem Segal, and Dalit Ben-Yosef. "Electrical maturation of neurons derived from human embryonic stem cells." F1000Research 3 (August 19, 2014): 196. http://dx.doi.org/10.12688/f1000research.4943.1.

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In-vitro neuronal differentiation of human pluripotent stem cells has become a widely used tool in disease modeling and prospective regenerative medicine. Most studies evaluate neurons molecularly and only a handful of them use electrophysiological tools to directly indicate that these are genuine neurons. Therefore, the specific timing of development of intrinsic electrophysiological properties and synaptic capabilities remains poorly understood. Here we describe a systematic analysis of developing neurons derived in-vitro from human embryonic stem cells (hESCs). We show that hESCs differentiated in-vitro into early embryonic neurons, displaying basically mature morphological and electrical features as early as day 37. This early onset of action potential discharges suggests that first stages of neurogenesis in humans are already associated with electrical maturation. Spike frequency, amplitude, duration, threshold and after hyperpolarization were found to be the most predictive parameters for electrical maturity. Furthermore, we were able to detect spontaneous synaptic activity already at these early time-points, demonstrating that neuronal connectivity can develop concomitantly with the gradual process of electrical maturation. These results highlight the functional properties of hESCs in the process of their development into neurons. Moreover, our results provide practical tools for the direct measurement of functional maturity, which can be reproduced and implemented for stem cell research of neurogenesis in general, and neurodevelopmental disorders in particular.

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Ngwenya, Laura B., Sarmistha Mazumder, Zachary R. Porter, Amy Minnema, Duane J. Oswald, and H. Francis Farhadi. "Implantation of Neuronal Stem Cells Enhances Object Recognition without Increasing Neurogenesis after Lateral Fluid Percussion Injury in Mice." Stem Cells International 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/4209821.

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Cognitive deficits after traumatic brain injury (TBI) are debilitating and contribute to the morbidity and loss of productivity of over 10 million people worldwide. Cell transplantation has been linked to enhanced cognitive function after experimental traumatic brain injury, yet the mechanism of recovery is poorly understood. Since the hippocampus is a critical structure for learning and memory, supports adult neurogenesis, and is particularly vulnerable after TBI, we hypothesized that stem cell transplantation after TBI enhances cognitive recovery by modulation of endogenous hippocampal neurogenesis. We performed lateral fluid percussion injury (LFPI) in adult mice and transplanted embryonic stem cell-derived neural progenitor cells (NPC). Our data confirm an injury-induced cognitive deficit in novel object recognition, a hippocampal-dependent learning task, which is reversed one week after NPC transplantation. While LFPI alone promotes hippocampal neurogenesis, as revealed by doublecortin immunolabeling of immature neurons, subsequent NPC transplantation prevents increased neurogenesis and is not associated with morphological maturation of endogenous injury-induced immature neurons. Thus, NPC transplantation enhances cognitive recovery early after LFPI without a concomitant increase in neuron numbers or maturation.

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Wu, Yahong, and Weiwei Zhang. "The Role of E3s in Regulating Pluripotency of Embryonic Stem Cells and Induced Pluripotent Stem Cells." International Journal of Molecular Sciences 22, no. 3 (January 25, 2021): 1168. http://dx.doi.org/10.3390/ijms22031168.

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Pluripotent embryonic stem cells (ESCs) are derived from early embryos and can differentiate into any type of cells in living organisms. Induced pluripotent stem cells (iPSCs) resemble ESCs, both of which serve as excellent sources to study early embryonic development and realize cell replacement therapies for age-related degenerative diseases and other cell dysfunction-related illnesses. To achieve these valuable applications, comprehensively understanding of the mechanisms underlying pluripotency maintenance and acquisition is critical. Ubiquitination modifies proteins with Ubiquitin (Ub) at the post-translational level to monitor protein stability and activity. It is extensively involved in pluripotency-specific regulatory networks in ESCs and iPSCs. Ubiquitination is achieved by sequential actions of the Ub-activating enzyme E1, Ub-conjugating enzyme E2, and Ub ligase E3. Compared with E1s and E2s, E3s are most abundant, responsible for substrate selectivity and functional diversity. In this review, we focus on E3 ligases to discuss recent progresses in understanding how they regulate pluripotency and somatic cell reprogramming through ubiquitinating core ESC regulators.

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Zhou, Yang, Qing-Song Dai, Shi-Chang Zhu, Yue-Hua Han, Hai-Long Han, Bo Zhao, Rong-Rong Gao, Jun Zhang, and Jing Zhang. "AK048794 maintains the mouse embryonic stem cell pluripotency by functioning as an miRNA sponge for miR-592." Biochemical Journal 473, no. 20 (October 11, 2016): 3639–54. http://dx.doi.org/10.1042/bcj20160540.

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MiR-592 has been identified as a neural-enriched microRNA, plays an important role in mNPCs differentiation, could induce astrogliogenesis differentiation arrest or/and enhance neurogenesis in vitro. Previous studies showed that long noncoding RNAs (lncRNAs) were involved in the neuronal development and activity. To investigate the role of miR-592 in neurogenesis, we described the expression profile of lncRNAs in miR-592 knockout mouse embryonic stem cells (mESCs) and the corresponding normal mESCs by microarray. By the microarray analysis and luciferase reporter assays, we demonstrated that lncRNA - AK048794, regulated by transcription factor GATA1, functioned as a competing endogenous RNA (ceRNA) for miR-592 and led to the de-repression of its endogenous target FAM91A1, which is involved in mESC pluripotency maintenance. Taken together, these observations imply that AK048794 modulated the expression of multiple genes involved in mESC pluripotency maintenance by acting as a ceRNA for miR-592, which may build up the link between the regulatory miRNA network and mESC pluripotency.

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Mohan, K. Naga. "Stem Cell Models to Investigate the Role of DNA Methylation Machinery in Development of Neuropsychiatric Disorders." Stem Cells International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/4379425.

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Epigenetic mechanisms underlie differentiation of pluripotent stem cells into different lineages that contain identical genomes but express different sets of cell type-specific genes. Because of high discordance rates in monozygotic twins, epigenetic mechanisms are also implicated in development of neuropsychiatric disorders such as schizophrenia and autism. In support of this notion, increased levels of DNA methyltransferases (DNMTs), DNMT polymorphisms, and dysregulation of DNA methylation network were reported among schizophrenia patients. These results point to the importance of development of DNA methylation machinery-based models for studying the mechanism of abnormal neurogenesis due to certain DNMT alleles or dysregulated DNMTs. Achieving this goal is strongly confronted by embryonic lethality associated with altered levels of epigenetic machinery such as DNMT1 and expensive approaches in developingin vivomodels. In light of literature evidence that embryonic stem cells (ESCs) are tolerant of DNMT mutations and advancement in the technology of gene targeting, it is now possible to introduce desired mutations in DNMT loci to generate suitable ESC lines that can help understand the underlying mechanisms by which abnormal levels of DNMTs or their specific mutations/alleles result in abnormal neurogenesis. In the future, these models can facilitate development of suitable drugs for treatment of neuropsychiatric disorders.

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Jawerka, Melanie, Dilek Colak, Leda Dimou, Carmen Spiller, Sabine Lagger, Rusty L. Montgomery, Eric N. Olson, Wolfgang Wurst, Martin Göttlicher, and Magdalena Götz. "The specific role of histone deacetylase 2 in adult neurogenesis." Neuron Glia Biology 6, no. 2 (April 14, 2010): 93–107. http://dx.doi.org/10.1017/s1740925x10000049.

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Gene expression changes during cell differentiation are thought to be coordinated by histone modifications, but still little is known about the role of specific histone deacetylases (HDACs) in cell fate decisions in vivo. Here we demonstrate that the catalytic function of HDAC2 is required in adult, but not embryonic neurogenesis. While brain development and adult stem cell fate were normal upon conditional deletion of HDAC2 or in mice lacking the catalytic activity of HDAC2, neurons derived from both zones of adult neurogenesis die at a specific maturation stage. This phenotype is correlated with an increase in proliferation and the aberrant maintenance of proteins normally expressed only in progenitors, such as Sox2, also into some differentiating neurons, suggesting that HDAC2 is critically required to silence progenitor transcripts during neuronal differentiation of adult generated neurons. This cell-autonomous function of HDAC2 exclusively in adult neurogenesis reveals clear differences in the molecular mechanisms regulating neurogenesis during development and in adulthood.

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Kim, Sun-Uk, Young-Ho Park, Jin-Man Kim, Hu-Nan Sun, In-Sung Song, Song Mei Huang, Sang-Hee Lee, et al. "Dominant Role of Peroxiredoxin/JNK Axis in Stemness Regulation During Neurogenesis from Embryonic Stem Cells." STEM CELLS 32, no. 4 (March 17, 2014): 998–1011. http://dx.doi.org/10.1002/stem.1593.

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Chen, Stephen, Andre B. H. Choo, Wang Nai-Dy, Too Heng-Phon, and Steve K. W. Oh. "Knockdown of Oct-4 or Sox-2 Attenuates Neurogenesis of Mouse Embryonic Stem Cells." Stem Cells and Development 16, no. 3 (June 2007): 413–20. http://dx.doi.org/10.1089/scd.2006.0099.

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Pei, Lijuan, Hongjie Zhang, Meihui Zhang, Yixuan Wang, and Ke Wei. "Rcor2 Is Required for Somatic Differentiation and Represses Germline Cell Fate." Stem Cells International 2022 (March 19, 2022): 1–11. http://dx.doi.org/10.1155/2022/5283615.

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Rcor2, the corepressor 2 of REST, a transcriptional repressor, is predominantly expressed in embryonic stem cells (ESCs) and plays a major role in regulating ESC pluripotency and neurogenesis. The function of Rcor2 in development of other germ layers is yet unclear. We utilized a Rcor2-/- mouse embryonic stem cell (mESC) line to investigate the role of Rcor2 in mESC differentiation. Rcor2-/- mESC shows reduced proliferation and severely compromised capacity to differentiate to all three germ layers. In contrast, Rcor2 knockout promotes primordial germ cells (PGCs) specific gene expression and possibly PGC formation. Mechanistically, we revealed that Rcor2 inhibits expression of genes required for PGC development, such as Dppa3 and Dazl, by associating to their promoters and enhancing local suppressive H3K9me3 modifications. Our results suggest that Rcor2 plays an important role in somatic cell fate determination by suppressing PGC differentiation through regulating epigenetic modifications of PGC specific genes.

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Han, Xinxin, Liming Yu, Jie Ren, Min Wang, Zhongliang Liu, Xinyu Hu, Daiyu Hu, et al. "Efficient and Fast Differentiation of Human Neural Stem Cells from Human Embryonic Stem Cells for Cell Therapy." Stem Cells International 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/9405204.

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Stem cell-based therapies have been used for repairing damaged brain tissue and helping functional recovery after brain injury. Aberrance neurogenesis is related with brain injury, and multipotential neural stem cells from human embryonic stem (hES) cells provide a great promise for cell replacement therapies. Optimized protocols for neural differentiation are necessary to produce functional human neural stem cells (hNSCs) for cell therapy. However, the qualified procedure is scarce and detailed features of hNSCs originated from hES cells are still unclear. In this study, we developed a method to obtain hNSCs from hES cells, by which we could harvest abundant hNSCs in a relatively short time. Then, we examined the expression of pluripotent and multipotent marker genes through immunostaining and confirmed differentiation potential of the differentiated hNSCs. Furthermore, we analyzed the mitotic activity of these hNSCs. In this report, we provided comprehensive features of hNSCs and delivered the knowledge about how to obtain more high-quality hNSCs from hES cells which may help to accelerate the NSC-based therapies in brain injury treatment.

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Mizushima, Noboru, Akitsugu Yamamoto, Masahiko Hatano, Yoshinori Kobayashi, Yukiko Kabeya, Kuninori Suzuki, Takeshi Tokuhisa, Yoshinori Ohsumi, and Tamotsu Yoshimori. "Dissection of Autophagosome Formation Using Apg5-Deficient Mouse Embryonic Stem Cells." Journal of Cell Biology 152, no. 4 (February 12, 2001): 657–68. http://dx.doi.org/10.1083/jcb.152.4.657.

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In macroautophagy, cytoplasmic components are delivered to lysosomes for degradation via autophagosomes that are formed by closure of cup-shaped isolation membranes. However, how the isolation membranes are formed is poorly understood. We recently found in yeast that a novel ubiquitin-like system, the Apg12-Apg5 conjugation system, is essential for autophagy. Here we show that mouse Apg12-Apg5 conjugate localizes to the isolation membranes in mouse embryonic stem cells. Using green fluorescent protein–tagged Apg5, we revealed that the cup-shaped isolation membrane is developed from a small crescent-shaped compartment. Apg5 localizes on the isolation membrane throughout its elongation process. To examine the role of Apg5, we generated Apg5-deficient embryonic stem cells, which showed defects in autophagosome formation. The covalent modification of Apg5 with Apg12 is not required for its membrane targeting, but is essential for involvement of Apg5 in elongation of the isolation membranes. We also show that Apg12-Apg5 is required for targeting of a mammalian Aut7/Apg8 homologue, LC3, to the isolation membranes. These results suggest that the Apg12-Apg5 conjugate plays essential roles in isolation membrane development.

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Endo, Makoto, Joseph E. Druso, and Richard A. Cerione. "The two splice variant forms of Cdc42 exert distinct and essential functions in neurogenesis." Journal of Biological Chemistry 295, no. 14 (February 18, 2020): 4498–512. http://dx.doi.org/10.1074/jbc.ra119.011837.

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The small GTPase cell division cycle 42 (CDC42) plays essential roles in neurogenesis and brain development. Previously, using murine embryonic P19 cells as a model system, we showed that CDC42 stimulates mTOR complex 1 (mTORC1) activity and thereby up-regulates transcription factors required for the formation of neural progenitor cells. However, paradoxically, although endogenous CDC42 is required for both the initial transition of undifferentiated P19 cells to neural progenitors and their ultimate terminal differentiation into neurons, ectopic CDC42 overexpression promotes only the first stage of neurogenesis (i.e. the formation of neuroprogenitors) and not the second phase (differentiation into neurons). Here, using both P19 cells and mouse embryonic stem cells, we resolve this paradox, demonstrating that two splice variants of CDC42, differing only in nine amino acid residues in their very C-terminal regions, play distinct roles in neurogenesis. We found that a CDC42 splice variant that has a ubiquitous tissue distribution, termed here as CDC42u, specifically drives the formation of neuroprogenitor cells, whereas a brain-specific CDC42 variant, CDC42b, is essential for promoting the transition of neuroprogenitor cells to neurons. We further show that the specific roles of CDC42u and CDC42b in neurogenesis are due to their opposing effects on mTORC1 activity. Specifically, CDC42u stimulated mTORC1 activity and thereby induced neuroprogenitor formation, whereas CDC42b worked together with activated CDC42-associated kinase (ACK) in down-regulating mTOR expression and promoting neuronal differentiation. These findings highlight the remarkable functional specificities of two highly similar CDC42 splice variants in regulating distinct stages of neurogenesis.

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Suresh, Bharathi, Junwon Lee, Kye-Seong Kim, and Suresh Ramakrishna. "The Importance of Ubiquitination and Deubiquitination in Cellular Reprogramming." Stem Cells International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/6705927.

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Ubiquitination of core stem cell transcription factors can directly affect stem cell maintenance and differentiation. Ubiquitination and deubiquitination must occur in a timely and well-coordinated manner to regulate the protein turnover of several stemness related proteins, resulting in optimal embryonic stem cell maintenance and differentiation. There are two switches: an E3 ubiquitin ligase enzyme that tags ubiquitin molecules to the target proteins for proteolysis and a second enzyme, the deubiquitinating enzyme (DUBs), that performs the opposite action, thereby preventing proteolysis. In order to maintain stemness and to allow for efficient differentiation, both ubiquitination and deubiquitination molecular switches must operate properly in a balanced manner. In this review, we have summarized the importance of the ubiquitination of core stem cell transcription factors, such as Oct3/4, c-Myc, Sox2, Klf4, Nanog, and LIN28, during cellular reprogramming. Furthermore, we emphasize the role of DUBs in regulating core stem cell transcriptional factors and their function in stem cell maintenance and differentiation. We also discuss the possibility of using DUBs, along with core transcription factors, to efficiently generate induced pluripotent stem cells. Our review provides a relatively new understanding regarding the importance of ubiquitination/deubiquitination of stem cell transcription factors for efficient cellular reprogramming.

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Zoungrana, Linda Ines, Meredith Krause-Hauch, Hao Wang, Mohammad Kasim Fatmi, Lauryn Bates, Zehui Li, Parth Kulkarni, Di Ren, and Ji Li. "The Interaction of mTOR and Nrf2 in Neurogenesis and Its Implication in Neurodegenerative Diseases." Cells 11, no. 13 (June 28, 2022): 2048. http://dx.doi.org/10.3390/cells11132048.

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Neurogenesis occurs in the brain during embryonic development and throughout adulthood. Neurogenesis occurs in the hippocampus and under normal conditions and persists in two regions of the brain—the subgranular zone (SGZ) in the dentate gyrus of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles. As the critical role in neurogenesis, the neural stem cells have the capacity to differentiate into various cells and to self-renew. This process is controlled through different methods. The mammalian target of rapamycin (mTOR) controls cellular growth, cell proliferation, apoptosis, and autophagy. The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) is a major regulator of metabolism, protein quality control, and antioxidative defense, and is linked to neurogenesis. However, dysregulation in neurogenesis, mTOR, and Nrf2 activity have all been associated with neurodegenerative diseases such as Alzheimer’s, Huntington’s, and Parkinson’s. Understanding the role of these complexes in both neurogenesis and neurodegenerative disease could be necessary to develop future therapies. Here, we review both mTOR and Nrf2 complexes, their crosstalk and role in neurogenesis, and their implication in neurodegenerative diseases.

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Berg, Daniel A., Allison M. Bond, Guo-li Ming, and Hongjun Song. "Radial glial cells in the adult dentate gyrus: what are they and where do they come from?" F1000Research 7 (March 5, 2018): 277. http://dx.doi.org/10.12688/f1000research.12684.1.

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Adult neurogenesis occurs in the dentate gyrus in the mammalian hippocampus. These new neurons arise from neural precursor cells named radial glia-like cells, which are situated in the subgranular zone of the dentate gyrus. Here, we review the emerging topic of precursor heterogeneity in the adult subgranular zone. We also discuss how this heterogeneity may be established during development and focus on the embryonic origin of the dentate gyrus and radial glia-like stem cells. Finally, we discuss recently developed single-cell techniques, which we believe will be critical to comprehensively investigate adult neural stem cell origin and heterogeneity.

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Aouadi, Myriam, Frédéric Bost, Leslie Caron, Kathiane Laurent, Yannick Le Marchand Brustel, and Bernard Binétruy. "p38 Mitogen-Activated Protein Kinase Activity Commits Embryonic Stem Cells to Either Neurogenesis or Cardiomyogenesis." Stem Cells 24, no. 5 (May 2006): 1399–406. http://dx.doi.org/10.1634/stemcells.2005-0398.

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Brown, Jared, Christopher Barry, Matthew T. Schmitz, Cara Argus, Jennifer M. Bolin, Michael P. Schwartz, Amy Van Aartsen, et al. "Interspecies chimeric conditions affect the developmental rate of human pluripotent stem cells." PLOS Computational Biology 17, no. 3 (March 1, 2021): e1008778. http://dx.doi.org/10.1371/journal.pcbi.1008778.

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Human pluripotent stem cells hold significant promise for regenerative medicine. However, long differentiation protocols and immature characteristics of stem cell-derived cell types remain challenges to the development of many therapeutic applications. In contrast to the slow differentiation of human stem cells in vitro that mirrors a nine-month gestation period, mouse stem cells develop according to a much faster three-week gestation timeline. Here, we tested if co-differentiation with mouse pluripotent stem cells could accelerate the differentiation speed of human embryonic stem cells. Following a six-week RNA-sequencing time course of neural differentiation, we identified 929 human genes that were upregulated earlier and 535 genes that exhibited earlier peaked expression profiles in chimeric cell cultures than in human cell cultures alone. Genes with accelerated upregulation were significantly enriched in Gene Ontology terms associated with neurogenesis, neuron differentiation and maturation, and synapse signaling. Moreover, chimeric mixed samples correlated with in utero human embryonic samples earlier than human cells alone, and acceleration was dose-dependent on human-mouse co-culture ratios. The altered gene expression patterns and developmental rates described in this report have implications for accelerating human stem cell differentiation and the use of interspecies chimeric embryos in developing human organs for transplantation.

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Beligala, Dilshan Harshajith, Arpan De, and Michael Eric Geusz. "A Meta-Analysis Characterizing Stem-Like Gene Expression in the Suprachiasmatic Nucleus and Its Circadian Clock." BioMed Research International 2018 (June 26, 2018): 1–11. http://dx.doi.org/10.1155/2018/3610603.

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Cells expressing proteins characteristic of stem cells and progenitor cells are present in the suprachiasmatic nucleus (SCN) of the adult mammalian hypothalamus. Any relationship between this distinctive feature and the master circadian clock of the SCN is unclear. Considering the lack of obvious neurogenesis in the adult SCN relative to the hippocampus and other structures that provide neurons and glia, it is possible that the SCN has partially differentiated cells that can provide neural circuit plasticity rather than ongoing neurogenesis. To test this possibility, available databases and publications were explored to identify highly expressed genes in the mouse SCN that also have known or suspected roles in cell differentiation, maintenance of stem-like states, or cell-cell interactions found in adult and embryonic stem cells and cancer stem cells. The SCN was found to have numerous genes associated with stem cell maintenance and increased motility from which we selected 25 of the most relevant genes. Over ninety percent of these stem-like genes were expressed at higher levels in the SCN than in other brain areas. Further analysis of this gene set could provide a greater understanding of how adjustments in cell contacts alter period and phase relationships of circadian rhythms. Circadian timing and its role in cancer, sleep, and metabolic disorders are likely influenced by genes selected in this study.

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Shukla, Mayuri, Areechun Sotthibundhu, and Piyarat Govitrapong. "Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease." Melatonin Research 3, no. 2 (June 1, 2020): 216–42. http://dx.doi.org/10.32794/mr11250059.

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The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.

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Chen, Hongwei, Yu Mao, Bin Li, Qiang Wei, Jinhuan Wang, Jianhong Wang, Shufen Wang, et al. "Neural lineage development of rhesus monkey embryonic stem cells: Insight of neurogenesis and gliogenesis in vitro." Cell Research 18, S1 (August 2008): S148. http://dx.doi.org/10.1038/cr.2008.238.

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Ghosh, Sukla, and Subhra Prakash Hui. "Regeneration of Zebrafish CNS: Adult Neurogenesis." Neural Plasticity 2016 (2016): 1–21. http://dx.doi.org/10.1155/2016/5815439.

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Regeneration in the animal kingdom is one of the most fascinating problems that have allowed scientists to address many issues of fundamental importance in basic biology. However, we came to know that the regenerative capability may vary across different species. Among vertebrates, fish and amphibians are capable of regenerating a variety of complex organs through epimorphosis. Zebrafish is an excellent animal model, which can repair several organs like damaged retina, severed spinal cord, injured brain and heart, and amputated fins. The focus of the present paper is on spinal cord regeneration in adult zebrafish. We intend to discuss our current understanding of the cellular and molecular mechanism(s) that allows formation of proliferating progenitors and controls neurogenesis, which involve changes in epigenetic and transcription programs. Unlike mammals, zebrafish retains radial glia, a nonneuronal cell type in their adult central nervous system. Injury induced proliferation involves radial glia which proliferate, transcribe embryonic genes, and can give rise to new neurons. Recent technological development of exquisite molecular tools in zebrafish, such as cell ablation, lineage analysis, and novel and substantial microarray, together with advancement in stem cell biology, allowed us to investigate how progenitor cells contribute to the generation of appropriate structures and various underlying mechanisms like reprogramming.

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Thiel, Gerald. "How Sox2 maintains neural stem cell identity." Biochemical Journal 450, no. 3 (February 28, 2013): e1-e2. http://dx.doi.org/10.1042/bj20130176.

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The transcription factor Sox2 [SRY (sex-determining region Y)-box 2] is expressed at the earliest developmental stages in the nervous system and functions as a marker protein for neural development. Sox2 is found in embryonic neural stem cells as well as in virtually all adult neural stem cells of the subventricular region and the subgranular zone of the hippocampus. Gain-of-function and loss-of-function experiments in transgenic animals revealed a key role for Sox2 in the maintenance of neural stem cell properties, including proliferation/survival, self-renewal and neurogenesis. A limited set of Sox2-responsive target genes have been identified, including the genes encoding the neural stem cell marker nestin and the signalling molecule sonic hedgehog. In this issue of the Biochemical Journal, Feng et al. identified the survivin gene as a target for Sox2 in neural stem cells. Survivin protects cells from programmed cell death and functions as a regulator of cell division. The regulation of survivin expression by Sox2 explains why the reduction of the Sox2 concentration in neural stem cells is accompanied by a reduced proliferation of the cells and an induction of apoptosis. It would be of interest to know whether the Sox2–survivin connection is a common scheme to maintain the ‘stemness’ identity of other stem/progenitor cells.

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Sato, Masahiro, Issei Saitoh, Yuki Kiyokawa, Yoko Iwase, Naoko Kubota, Natsumi Ibano, Hirofumi Noguchi, Youichi Yamasaki, and Emi Inada. "Tissue-Nonspecific Alkaline Phosphatase, a Possible Mediator of Cell Maturation: Towards a New Paradigm." Cells 10, no. 12 (November 28, 2021): 3338. http://dx.doi.org/10.3390/cells10123338.

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Alkaline phosphatase (ALP) is a ubiquitous membrane-bound glycoprotein capable of providing inorganic phosphate by catalyzing the hydrolysis of organic phosphate esters, or removing inorganic pyrophosphate that inhibits calcification. In humans, four forms of ALP cDNA have been cloned, among which tissue-nonspecific ALP (TNSALP) (TNSALP) is widely distributed in the liver, bone, and kidney, making it an important marker in clinical and basic research. Interestingly, TNSALP is highly expressed in juvenile cells, such as pluripotent stem cells (i.e., embryonic stem cells and induced pluripotent stem cells (iPSCs)) and somatic stem cells (i.e., neuronal stem cells and bone marrow mesenchymal stem cells). Hypophosphatasia is a genetic disorder causing defects in bone and tooth development as well as neurogenesis. Mutations in the gene coding for TNSALP are thought to be responsible for the abnormalities, suggesting the essential role of TNSALP in these events. Moreover, a reverse-genetics-based study using mice revealed that TNSALP is important in bone and tooth development as well as neurogenesis. However, little is known about the role of TNSALP in the maintenance and differentiation of juvenile cells. Recently, it was reported that cells enriched with TNSALP are more easily reprogrammed into iPSCs than those with less TNSALP. Furthermore, in bone marrow stem cells, ALP could function as a “signal regulator” deciding the fate of these cells. In this review, we summarize the properties of ALP and the background of ALP gene analysis and its manipulation, with a special focus on the potential role of TNSALP in the generation (and possibly maintenance) of juvenile cells.

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Varghese, Divya S., Shama Parween, Mustafa T. Ardah, Bright Starling Emerald, and Suraiya A. Ansari. "Effects of Aminoglycoside Antibiotics on Human Embryonic Stem Cell Viability during Differentiation In Vitro." Stem Cells International 2017 (2017): 1–18. http://dx.doi.org/10.1155/2017/2451927.

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Human embryonic stem cells (hESCs) are being used extensively in array of studies to understand different mechanisms such as early human embryogenesis, drug toxicity testing, disease modeling, and cell replacement therapy. The protocols for the directed differentiation of hESCs towards specific cell types often require long-term cell cultures. To avoid bacterial contamination, these protocols include addition of antibiotics such as pen-strep and gentamicin. Although aminoglycosides, streptomycin, and gentamicin have been shown to cause cytotoxicity in various animal models, the effect of these antibiotics on hESCs is not clear. In this study, we found that antibiotics, pen-strep, and gentamicin did not affect hESC cell viability or expression of pluripotency markers. However, during directed differentiation towards neural and hepatic fate, significant cell death was noted through the activation of caspase cascade. Also, the expression of neural progenitor markers Pax6, Emx2, Otx2, and Pou3f2 was significantly reduced suggesting that gentamicin may adversely affect early embryonic neurogenesis whereas no effect was seen on the expression of endoderm or hepatic markers during differentiation. Our results suggest that the use of antibiotics in cell culture media for the maintenance and differentiation of hESCs needs thorough investigation before use to avoid erroneous results.

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Yu, Hui-Mei, Jing Wen, Rong Wang, Wan-Hua Shen, Shumin Duan, and Huang-Tian Yang. "Critical role of type 2 ryanodine receptor in mediating activity-dependent neurogenesis from embryonic stem cells." Cell Calcium 43, no. 5 (May 2008): 417–31. http://dx.doi.org/10.1016/j.ceca.2007.07.006.

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Journal articles on the topic 'Neurogenesis; ubiquitin; embryonic stem cell'

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