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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Plant, cell & environment 27 (2004), S. 0 
    ISSN: 1365-3040
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Jasmonic acid (JA) is known to be involved in the response of plants to environmental stresses such as drought, and betaine (glycinebetaine) is an osmopretectant accumulated in plants under environmental stresses including drought. However, it remains currently unclear whether JA is involved in the water-stress-induced betaine accumulation in plant leaves. The present experiment, performed with the whole pear plant (Pyrus bretschneideri Redh. cv. Suli), revealed that the exogenously applied JA induced a significant increase of the betaine level in the pear leaves when the plants were not yet stressed by drought, and when the plants were subjected to water stress, the ‘JA plus drought’ treatment induced a significant higher betaine level than did the drought treatment alone. Meanwhile, the ‘JA plus drought’ treatment induced higher levels of betaine aldehyde dehydrogenase (BADH, E C 1.2.1.8) and activities in the leaves than did the drought treatment alone. These results obtained in the whole plant experiments were supported by the results of detached leaf experiments. In detached leaves JA induced significant increases in betaine levels, BADH activities and BADH protein amounts in a time- and concentration-dependent manner. These data demonstrate that JA is involved in the drought-induced betaine accumulation in pear leaves.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Macmillian Magazines Ltd.
    Nature 411 (2001), S. 669-671 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Understanding the complexities of electronic and magnetic ground states in solids is one of the main goals of solid-state physics. Transition-metal oxides have proved to be particularly fruitful in this regard, especially for those materials with the perovskite structure, where the special ...
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2015-03-26
    Description: Objective— Transient receptor potential melastatin-2 (TRPM2) channel is a nonselective cation channel that mediates influx of Ca 2+ and Na + with relative permeability of P Ca: P Na 0.6 in response to cellular oxidative stress. As angiogenesis and ischemic neovascularization are both significantly dependent on oxidant signaling, here we investigated the possible role of vascular endothelial growth factor (VEGF)–induced reactive oxygen species production in activating TRPM2-dependent Ca 2+ signaling and in the mechanism of angiogenesis and ischemic neovascularization. Approach and Results— We observed that VEGF stimulation rapidly induced the association of TRPM2 and cellular Src kinase with vascular endothelial-cadherin forming a signalplex at vascular endothelial-cadherin junctions in endothelial cells. Using endothelial cells isolated from TRPM2 –/– mice or after small interfering RNA depletion of TRPM2, we demonstrated that TRPM2-activated Ca 2+ signaling was required for cellular Src kinase–induced phosphorylation of vascular endothelial-cadherin at Y658 and Y731, the crucial sites involved in vascular endothelial-cadherin internalization in response to VEGF. VEGF-induced reactive oxygen species generation activated TRPM2-induced Ca 2+ entry, whereas the reactive oxygen species–insensitive TRPM2 mutant (C1008-〉A) showed impaired Ca 2+ entry. Endothelial cells depleted of TRPM2 also displayed significantly perturbed migratory phenotype and impaired activation of cellular Src in response to VEGF. TRPM2 –/– mice reconstituted with wild-type myeloid cells demonstrated aberrant angiogenesis and neovascularization in the hindlimb ischemia model as compared with wild-type mice. Conclusions— VEGF-induced angiogenesis and postischemic neovascularization in mice required reactive oxygen species generation in endothelial cells and resultant TRPM2 activation. Thus, our findings provide novel insight into the role of TRPM2 in mechanism of angiogenesis and ischemic neovascularization.
    Keywords: Angiogenesis, Other Vascular biology
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
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  • 4
    Publication Date: 2012-08-31
    Description: Rationale: Adherens junctions (AJs) are the primary intercellular junctions in microvessels responsible for endothelial barrier function. Homophilic adhesion of vascular endothelial (VE) cadherin forms AJs, which are stabilized by binding of p120-catenin (p120). p120 dissociation from VE-cadherin results in loss of VE-cadherin homotypic interaction and AJ disassembly; however, the signaling mechanisms regulating p120 dissociation from VE-cadherin are not understood. Objective: To address the mechanism of protein kinase C (PKC)-α function in increasing endothelial permeability, we determined the role of PKCα phosphorylation of p120 in mediating disruption of AJ integrity. Methods and Results: We showed that PKCα phosphorylation of p120 at serine (S)879 in response to thrombin or lipopolysaccharide challenge reduced p120 binding affinity for VE-cadherin and mediated AJ disassembly secondary to VE-cadherin internalization. In studies in mouse lung vessels, expression of the phosphodeficient S879A-p120 mutant prevented the increase in vascular permeability induced by activation of the thrombin receptor PAR-1. Conclusions: PKCα phosphorylation of p120 at S879 is a critical phospho-switch mediating disassociation of p120 from VE-cadherin that results in AJ disassembly. Therefore, blocking PKCα-mediated p120 phosphorylation represents a novel targeted anti-inflammatory strategy to prevent disruption of vascular endothelial barrier function.
    Keywords: Thrombin, Endothelium/vascular type/nitric oxide
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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