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  • 1
    Electronic Resource
    Electronic Resource
    Activity-dependent neurotrophic factor: a potent regulator of embryonic growth and development (1999)
    Springer
    Anatomy and embryology 200 (1999), S. 65-71 
    Details
    ISSN: 1432-0568
    Keywords: Key words Mouse ; Vasoactive intestinal peptide ; Postimplantation ; Growth factor ; Embryogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Activity-dependent neurotrophic factor is a potent, neuroprotective molecule released from astroglia following stimulation by vasoactive intestinal peptide and, at least in part, accounts for the neuroprotective actions of vasoactive intestinal peptide. As well as enhancing neuronal survival, vasoactive intestinal peptide is known to regulate embryonic growth during the early postimplantation period of development. The current study was designed to assess activity-dependent neurotrophic factor’s role in the growth-regulatory properties of vasoactive intestinal peptide. Treatment of whole cultured day-9 mouse embryos with activity-dependent neurotrophic factor (10–13 M) resulted in a growth of 3.1 somites, compared with 1.6 somites in control embryos after a 4 h incubation period. Significant increases were also seen in cross-sectional area, protein and DNA content and bromodeoxyuridine incorporation. Activity-dependent neurotrophic factor-treated embryos were morphologically indistinguishable from control embryos of the same size. Anti-activity-dependent neurotrophic factor ascites significantly inhibited growth. In addition, co-treatment of embryos with anti-activity-dependent neurotrophic factor ascites inhibited vasoactive intestinal peptide-stimulated growth. Although anti-vasoactive intestinal peptide treatment inhibited growth, it did not inhibit activity-dependent neurotrophic factor-induced growth. These data indicate that an activity-dependent neurotrophic factor-like substance is an endogenous and potent growth-promoting factor in the early postimplantation embryo and that vasoactive intestinal peptide-regulated growth of embryos occurs, at least in part, through the action of activity-dependent neurotrophic factor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004290050260
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  • 2
    Electronic Resource
    Electronic Resource
    Potent mammalian cerebroprotection and neuronal cell death inhibition are afforded by a synthetic antioxidant analogue of marine invertebrate cell protectant ovothiols (2003)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 18 (2003), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Implicit strategies for neuroprotection in the adult brain include GABAA receptor activation, N-methyl-d-aspartate receptor and sodium voltage-gated channel inhibition. Ironically, these same targets may be harmful to the immature or developing brain. Protection has been demonstrated for both immature and mature brain with the use of a synthetic ovothiol analogue. The following beneficial effects have been demonstrated in mice: protection against audiogenic seizures, brain structures with clear-cut delineation of ibotenate-challenged white and grey matter lesions along with exceptional early and delayed protections, and potent cerebral cell death inhibition. The compound lacks both GABAergic activity and sodium channel blocker properties, which may help explain the lack of toxicity normally expressed in an immature brain utilizing these agents [J.W. Olney (2002) Neurotoxicology, 93, 1–10]. The oxidized form of the compound is virtually devoid of antioxidant activity. In vivo it exhibits cerebroprotective properties similar to those of reduced compounds endowed with antioxidant properties. This unexpected finding has prompted an extensive in vitro exploration of underlying molecular mechanisms that have led to the identification of several recycling mechanisms consistent with non rate-limiting conversion of oxidized to reduced compound forms. Taken as a whole, this work offers an unique combined in vitro and in vivo support that: (i) antioxidant therapy, here engineered from marine invertebrate egg protectants, may be a valuable strategy in protecting both mammalian adult and developing brain; and (ii) recycling (thiol-disulphide exchange) properties of the oxidized form of an antioxidant compound are as important as the antioxidant potential exhibited by a bioactive reduced antioxidant in certain neuroprotective processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2003.02846.x
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  • 3
    Electronic Resource
    Electronic Resource
    VIP and PACAP induce selective neuronal differentiation of mouse embryonic stem cells (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 19 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The capacity of embryonic stem cells (ES cells) to differentiate into neuronal cells represents a potential source for neuronal replacement and a model for studying factors controlling early stages of neuronal differentiation. Various molecules have been used to induce such differentiation but so far neuropeptides acting via functional G-protein-coupled receptors (GPCRs) have not been investigated. Vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are neuropeptides expressed in early development which affect neuronal precursor proliferation and neuronal differentiation. VIP and PACAP share two common receptors (VPAC1 and VPAC2 receptors) while only PACAP binds with high affinity to PAC1 receptors. The aim of the study was to determine whether VIP and PACAP could produce functional neuronal differentiation of ES cells. Mouse ES cells were allowed to aggregate in embryoid bodies (EBs) in the presence or not of VIP and PACAP for 1 week. VIP and PACAP potently increased the proportion of EB-derived cells expressing specifically a neuronal phenotype shown by immunocytochemistry and neurite outgrowth without altering glial cell number. Binding and RT-PCR analyses demonstrated the presence of VPAC2 and PAC1 receptors on ES cells. Accordingly, both peptides increased cyclic AMP and intracellular calcium. In contrast, EB-derived cells only expressed a functional PAC1 receptor, suggesting a switch in GPCR phenotype during ES cell differentiation. These original data demonstrate that functional GPCRs for VIP and PACAP are present on ES cells and that these neuropeptides may induce their differentiation into a neuronal phenotype. It opens an exciting new field for neuropeptide regulation of tissue ontogenesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0953-816X.2004.03138.x
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  • 4
    Electronic Resource
    Electronic Resource
    Vasoactive intestinal peptide shortens both G1 and S phases of neural cell cycle in whole postimplantation cultured mouse embryos (1998)
    Oxford, UK : Blackwell Science, Ltd
    European journal of neuroscience 10 (1998), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Vasoactive intestinal peptide, a trophic and mitogenic factor, stimulates growth in whole cultured mouse embryos. Inhibition of this growth function between embryonic days 9 and 11 induces growth retardation accompanied by severe microcephaly. In the present study, to determine the effects of this peptide on the different phases of the cell cycle of neural cells, embryonic day 9.5 cultured mouse embryos were cumulatively labelled with bromodeoxyuridine. Vasoactive intestinal peptide (10–7m) shortened S phase and G1 phase of neuroepithelial cells by 50% (4.8–2.4 h) and 58% (1.9–0.8 h), respectively, compared with controls. G2 and M phases were not modified by vasoactive intestinal peptide treatment. Total cell cycle length was consequently reduced by 43% (8.2–4.7 h) in vasoactive intestinal peptide treated embryos, compared with controls. In contrast, vasoactive intestinal peptide did not modify the rate of neuroepithelial cell death as assessed by the proportion of nuclei containing fragmented DNA. These data suggest that vasoactive intestinal peptide stimulates growth in premigratory stages of nervous system development by shortening S and G1 phases of the cell cycle and that S phase duration can be regulated by a physiological peptide.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1998.00172.x
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  • 5
    Electronic Resource
    Electronic Resource
    Regulation of Neuroprotective Action of Vasoactive Intestinal Peptide in the Murine Developing Brain by Protein Kinase C and Mitogen-Activated Protein Kinase Cascades: In Vivo and In Vitro Studies (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Intracerebral administration of the excitotoxin ibotenate to newborn mice induces white matter lesions mimicking periventricular leukomalacia, the most frequent brain lesion occurring in premature human babies. In this model, coinjection of vasoactive intestinal peptide prevents white matter lesions. In the present study, coadministration of ibotenate, vasoactive intestinal peptide, and selective transduction inhibitors showed that protein kinase C and mitogen-associated protein kinase pathways were critical for neuroprotection. In vivo and in vitro immunocytochemistry revealed that vasoactive intestinal peptide activated protein kinase C in astrocytes and neurons, and mitogen-associated protein kinase in neurons. In vitro neuronal transduction activation was indirect and required medium conditioned by astrocytes in which protein kinase C had been activated by vasoactive intestinal peptide. Although vasoactive intestinal peptide did not prevent the initial in vivo appearance of white matter lesion, it promoted a secondary repair of this lesion with axonal regrowth. Through protein kinase C activation, vasoactive intestinal peptide also prevented ibotenate-induced white matter astrocyte death. These data support the following hypothetical model: Vasoactive intestinal peptide activates protein kinase C in astrocytes, which promotes astrocytic survival and release of soluble factors; these released factors activate neuronal mitogen-associated protein kinase and protein kinase C, which will permit axonal regrowth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70062574.x
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  • 6
    Electronic Resource
    Electronic Resource
    Involvement of Pituitary Adenylate Cyclase-Activating Polypeptide II Vasoactive Intestinal Peptide 2 Receptor in Mouse Neocortical Astrocytogenesis (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: At the end of neuronal migration, the neopallial germinative zone produces glial cells destined to colonize the upper layers of neocortex. High densities of binding sites for vasoactive intestinal peptide (VIP) have been found in the rodent germinative zone just after completion of neuronal migration, suggesting a possible role of VIP in neocortical astrocytogenesis. In the present study, administration of a VIP antagonist at embryonic days 17 and 18 to pregnant mice was followed by a dramatic depletion of astrocytes in the upper cortical layer of the offspring. The depletion of astrocytes was dose-dependent, with a 42% reduction in the density of astrocytes observed with 50 µg of antagonist. The antagonist effect was reversed by cotreatment with VIP or pituitary adenylate cyclase-activating polypeptide (PACAP), suggesting the involvement of a receptor common to these two neuropeptides. VIP antagonist-induced inhibition of astrocytogenesis was also blocked by Ro 25-1553, a long-acting cyclic VIP analogue selective for the PACAP II VIP2 receptor subclass. Our results demonstrate that VIP and/or PACAP play a crucial physiological role in neocortical astrocytogenesis, possibly through interaction with PACAP II VIP2 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70052165.x
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  • 7
    Electronic Resource
    Electronic Resource
    Growth factor function of vasoactive intestinal peptide in whole cultured mouse embryos (1993)
    [s.l.] : Nature Publishing Group
    Nature 362 (1993), S. 155-158 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] FIG. 1 VIP stimulates the growth of whole cultured embryos when compared with medium alone (C) or secretin (S). In each group, a total of 5-18 embryos that had been processed in at least three separate experiments were included. Bar represents mean ±s.e.m.; asterisks indicate difference from ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/362155a0
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  • 8
    Electronic Resource
    Electronic Resource
    Role of tissue factor in embryonic blood vessel development (1996)
    [s.l.] : Nature Publishing Group
    Nature 383 (1996), S. 73-75 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Targeted disruption of the TF gene was accomplished by deleting transcriptional and translational start signals (Fig. la). Genotyping of offspring (Fig. Ib) from TF+/~ mice indicated that the targeted TF allele was inherited in a mendelian pattern, but that TF'1' embryos died in utero between ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/383073a0
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  • 9
    Electronic Resource
    Electronic Resource
    A mouse model for Zellweger syndrome (1997)
    [s.l.] : Nature Publishing Group
    Nature genetics 17 (1997), S. 49-57 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The cerebro-hepato-renal syndrome of Zellweger is a fatal inherited disease caused by deficient import of peroxisomal matrix proteins. The pathogenic mechanisms leading to extreme hypotonia, severe mental retardation and early death are unknown. We generated a Zellweger animal model through ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0997-49
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