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  • American Physiological Society  (2)
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  • American Physiological Society  (2)
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  • 1
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 283, No. 4 ( 2002-10-01), p. R964-R971
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 283, No. 4 ( 2002-10-01), p. R964-R971
    Kurzfassung: Antagonists to the N-methyl-d-aspartate (NMDA) receptor bind to various extraneuronal tissues. We therefore assessed the expression of the main NMDA subunit, NR1, in various tissues. We demonstrate that NR1 appears to be most abundant in the rat kidney and heart. NR1 is present in total rat kidney, cortex, and medulla. Of the NR2 subunits, only the NR2C subunit protein is present in the kidney. The abundance of the NR1 subunit protein increases with kidney development. Both NR1 and NR2C are present in opossum kidney, Madin-Darby canine kidney, and LLC-PK 1 cells. Immunohistochemistry studies show that the NR1 subunit is present in the renal proximal tubule. NR1 is abundant in the atrium and ventricle but is also expressed in the aorta and pulmonary artery. The NR2 subunits are not expressed in the heart. NR1 subunit protein expression is constant throughout heart development. Finally, the NR1 subunit protein is expressed in heart cells (H9c2) grown in culture. These studies reveal the presence of the NMDA receptor in the kidney and the cardiovascular system.
    Materialart: Online-Ressource
    ISSN: 0363-6119 , 1522-1490
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2002
    ZDB Id: 1477297-8
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 2018
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 315, No. 2 ( 2018-08-01), p. L286-L300
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 315, No. 2 ( 2018-08-01), p. L286-L300
    Kurzfassung: Using confocal microscopy, we quantitatively assessed uptake, processing, and egress of near-infrared (NIR)-labeled carboxylated polystyrene nanoparticles (PNP) in live alveolar epithelial cells (AEC) during interactions with primary rat AEC monolayers (RAECM). PNP fluorescence intensity (content) and colocalization with intracellular vesicles in a cell were determined over the entire cell volume via z stacking. Isotropic cuvette-based microfluorimetry was used to determine PNP concentration ([PNP]) from anisotropic measurements of PNP content assessed by confocal microscopy. Results showed that PNP uptake kinetics and steady-state intracellular content decreased as diameter increased from 20 to 200 nm. For 20-nm PNP, uptake rate and steady-state intracellular content increased with increased apical [PNP] but were unaffected by inhibition of endocytic pathways. Intracellular PNP increasingly colocalized with autophagosomes and/or lysosomes over time. PNP egress exhibited fast Ca 2+ concentration-dependent release and a slower diffusion-like process. Inhibition of microtubule polymerization curtailed rapid PNP egress, resulting in elevated vesicular and intracellular PNP content. Interference with autophagosome formation led to slower PNP uptake and markedly decreased steady-state intracellular content. At steady state, cytosolic [PNP] was higher than apical [PNP] , and vesicular [PNP] (~80% of intracellular PNP content) exceeded both cytosolic and intracellular [PNP] . These data are consistent with the following hypotheses: 1) autophagic processing of nanoparticles is essential for maintenance of AEC integrity; 2) altered autophagy and/or lysosomal exocytosis may lead to AEC injury; and 3) intracellular [PNP] in AEC can be regulated, suggesting strategies for enhancement of nanoparticle-driven AEC gene/drug delivery and/or amelioration of AEC nanoparticle-related cellular toxicity.
    Materialart: Online-Ressource
    ISSN: 1040-0605 , 1522-1504
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2018
    ZDB Id: 1477300-4
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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