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  • 1
    Keywords: CELLS ; GROWTH ; BLOOD ; GENE ; MATURATION ; DISRUPTION ; EXPRESSION ANALYSIS ; TUMOR ANGIOGENESIS ; MORPHOGENESIS ; neuropilin-1
    Abstract: OBJECTIVE: To characterize the role of a vascular-expressed class 3 semaphorin (semaphorin 3G [Sema3G]). METHODS AND RESULTS: Semaphorins have been identified as axon guidance molecules. Yet, they have more recently also been characterized as attractive and repulsive regulators of angiogenesis. Through a transcriptomic screen, we identified Sema3G as a molecule of angiogenic endothelial cells. Sema3G-deficient mice are viable and exhibit no overt vascular phenotype. Yet, LacZ expression in the Sema3G locus revealed intense arterial vascular staining in the angiogenic vasculature, starting at E9.5, which was detectable throughout adolescence and downregulated in adult vasculature. Sema3G is expressed as a full-length 100-kDa secreted molecule that is processed by furin proteases to yield 95- and a 65-kDa Sema domain-containing subunits. Full-length Sema3G binds to NP2, whereas processed Sema3G binds to NP1 and NP2. Expression profiling and cellular experiments identified autocrine effects of Sema3G on endothelial cells and paracrine effects on smooth muscle cells. CONCLUSIONS: Although the mouse knockout phenotype suggests compensatory mechanisms, the experiments identify Sema3G as a primarily endothelial cell-expressed class 3 semaphorin that controls endothelial and smooth muscle cell functions in autocrine and paracrine manners, respectively.
    Type of Publication: Journal article published
    PubMed ID: 20947821
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  • 2
    ISSN: 1432-1106
    Keywords: Preoptic area ; Opioid binding ; Diprenorphine ; Noradrenergic transmission ; Ventral noradrenergic tract lesion ; Autoradiography ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were undertaken to establish whether opioid receptors exert a direct presynaptic influence on noradrenergic (NA) terminals in the preoptic/ anterior hypothalamus (PO/AH) of the female rat. Thus, opioid binding studies were performed in rats with lesions of the ventral NA tract (VNAT; the main NA projection to the hypothalamus) to assess whether a loss of NA terminals may also result in a decrease in opioid binding in the PO/AH. In the first experiment, unilateral electrolytic lesions of the VNAT caused a significant reduction in both the NA content and specific [3H]-diprenorphine binding to membrane homogenates in the ipsilateral PO/AH. In the second experiment bilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the VNAT caused a significant reduction in NA levels in the PO/AH as well as significant decreases in the density of [3H]-diprenorphine binding to tissue sections of the PO/AH when compared to control animals. These results strongly suggest that the NA input to the PO/AH is regulated by endogenous opioid peptides, and provide an anatomical substrate to explain opioid-NA interactions in the control of gonadotrophin releasing hormone (GnRH) and gonadotrophin secretion.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1106
    Keywords: Opioids enkephalins supraoptic ; Nucleus oxytocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary When electrical stimuli are applied to the neural stalk of the pituitary, oxytocin, vasopressin, and probably several opioid peptides also contained in nerve terminals in the gland are released: one action of the released opioids appears to be to inhibit oxytocin release by an action that has been likened to pre-synaptic inhibition. Thus, when Clarke et al. (1979) stimulated the neural stalk following intravenous injection of the opioid antagonist naloxone, they observed that the evoked oxytocin release was potentiated. In the present study we confirm this result and show that oxytocin release evoked by stimulation of the supraoptic nucleus is similarly potentiated by naloxone. This finding is consistent with the hypothesis that the opioid responsible for inhibition of oxytocin release coexists with either oxytocin or vasopressin. We further report that the specific δ-receptor antagonist ICI 174864 does not potentiate oxytocin release either in vivo or in vitro. Thus, it seems unlikely that the enkephalins, putative δ-receptor agonists present in neurohypophysial fibres, are the opioids responsible for the observed inhibition of oxytocin release.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2145
    Keywords: Key words Apomixis ; Apospory ; Hieracium ; Seed ; Modifiers ; Adventitious embryony
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract  Apomixis is facultative in characterized members of the genus Hieracium. The three components that comprise the apomictic mechanism include apospory followed by autonomous embryo and endosperm formation. The time of aposporous embryo sac initiation and mode of embryo sac formation are different in Hieracium piloselloides (D3) and Hieracium aurantiacum (A3.4). Genetic studies have shown that a single dominant locus encodes all three components of apomixis in both species (Bicknell et al. 2000). We histologically examined a range of related, genetically characterized apomictic Hieracium plants derived from D3 and A3.4 to assess conservation of the apomictic mechanism in different genetic backgrounds. The plants varied in ploidy, and also in the amount of DNA introduced from sexual Hieracium pilosella (P4). An apomictic hybrid from a cross between the two apomicts was also examined. The developmental processes observed in the parental apomicts were not conserved in the examined plants and alterations occurred in the components of apomixis. One plant also exhibited adventitious embryony. The results show that other genetic factors can modify apomixis with respect to time of initiation, spatial location, and mode of developmental progression. Both the apomictic locus and the modifiers are essential for efficient penetrance of the trait in Hieracium. Some of the findings in Hieracium correspond with observations in Ranunculus and this is discussed in terms of models for apomictic development and the control of apomixis in crops.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Considerable evidence indicates that the microvascular changes observed in psoriasis are a result of angiogenesis. Vascular proliferation is driven by the local production of molecules which have angiogenic activity. Platelet-derived endothelial cell growth factor/thymidine phosphorylase (PDECGF/TP) is a potent angiogenic factor active in in vivo angiogenesis assays and overexpressed in several tumour types. We have demonstrated by ribonuclease protection analysis a consistently high degree of PDECGF/TP mRNA production in lesional psoriatic skin, while immunohistochemical studies revealed strong PDECGF/TP immunoreactivity in lesional epidermis, with nuclear staining present in basal keratinocytes and cytoplasmic immunoreactivity in suprabasal layers. Non-lesional skin showed minimal PDECGF/TP mRNA production and weak epidermal immunostaining. These results indicate a potential role for PDECGF/TP in the pathophysiology of psoriasis, and reveal a target for antiangiogenesis therapy in the treatment of this disease.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 298 (1982), S. 161-162 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] For each experiment the neurohypophysis was dissected from a freshly decapitated male Wistar rat, and impaled on one of a pair of sharpened platinum/iridium stimulating electrodes6. The electrode assembly was inserted in a small Perspex chamber, and the gland was continuously perifused at 37 C with ...
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science, Ltd
    Journal of neuroendocrinology 14 (2002), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Opioid peptides are present in nerve terminals in the rat neural lobe where they partially coexist with vasopressin. Morphological findings suggest that these neuropeptides are released onto pituicytes, which is in agreement with a possible role for the pituicyte in oxytocin and vasopressin release from the neural lobe.Pituicytes in culture respond to vasopressin with a mobilization of calcium from intracellular stores. In the present study this vasopressin induced increase in intracellular free calcium levels was both delayed and decreased by pre-exposure to dynorphin 1–17, while dynorphin 1–17 by itself did not affect basal calcium levels. All effects of dynorphin 1–17 could be blocked with naloxone. The present results suggest that opioid receptors are present on pituicytes and are coupled to a second messenger pathway by which opioid peptides may inhibit inositol phosphate dependent calcium mobilization by other neuropeptides, such as vasopressin.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have investigated the influence of endogenous opioids on oxytocin secretion during pregnancy. In blood-sampled consciousrats on days 18 and 21 of pregnancy plasma oxytocin concentration, measured by radioimmunoassay, was significantly increased compared to non-pregnant or post-partum rats. On days 15, 18 and 21 of pregnancy, but not in non-pregnant, early pregnant or post-partum rats, the opioid antagonist naloxone caused a significant increase in plasma oxytocin compared to vehicle injection, indicating activation of an endogenous opioid restraint over oxytocin secretion.Electrically stimulated neural lobes isolated from 16- and 21-day pregnant rats released more oxytocin than those from non-pregnant rats. However, naloxone (10−5 M) was less effective at potentiating, and the k-opioid agonist U50,488 (10−5 M) was less effective at inhibiting, stimulated release at the end of pregnancy than in non-pregnant rats suggesting desensitization of oxytocin nerve terminals to actions of endogenous opioids. Neural lobes from male rats drinking 2% saline for 4 days also showed desensitization of oxytocin nerve endings to naloxone.Neither neural lobe content of dynorphin A(1–8), an endogenous k-opioid, nor prodynorphin mRNA expression, measured by in situ hybridization histochemistry in the supraoptic nucleus altered during pregnancy. However, neural lobe content of Met5enkephalin significantly decreased by day 21 of gestation suggesting enhanced release. We conclude that an endogenous opioid, possibly a product of proenkephalin A in oxytocin cells may be responsible for auto-inhibition of oxytocin release during gestation, and that this mechanism desensitizes in late pregnancy at a time when other opioid inputs to the oxytocin neurons become activated to provide an overall increase in opioid restraint of the system. The changes in opioid input through pregnancy may be involved in initiation and regulation of oxytocin secretion at parturition. A similar opioid mechanism, but possibly involving dynorphin, could explain desensitization in saline drinking rats and indicates that desensitization may be a consequence of chronic activation of secretion from the oxytocin nerve terminals rather than a phenomenon peculiar to pregnancy.
    Type of Medium: Electronic Resource
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