Archives of Histology and Cytology
Online ISSN : 1349-1717
Print ISSN : 0914-9465
ISSN-L : 0914-9465
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  • Kinue Shimizu, Megumi Sano, Aoi Kita, Nobuhiko Sawai, Akiko Iizuk ...
    2017 Volume 77 Issue 1 Pages 25-38
    Published: October 26, 2017
    Released: October 26, 2017

    Summary. Aquaporin-2 (AQP2) is a water channel protein that is trafficked between intracellular vesicles and the plasma membrane of kidney collecting duct cells upon vasopressin stimulation. Vasopressin changes the phosphorylation states of the AQP2 C-terminal serines (Sers), Ser256, Ser261, Ser264, and Ser269, in rats and mice, which is thought to play a role in controlling trafficking. Here, we focused on Ser269. We developed a specific antibody to Ser269-phosphorylated AQP2. Using immunofluorescence microscopy, we examined its localization in the rat kidney following injection of vasopressin and a vasopressin type 2 receptor-specific antagonist (OPC-31260). Ser269-phosphorylated AQP2 was almost undetectable in the water-loaded rat kidney, but was detected intracellularly soon after vasopressin injection, and then highly accumulated on the apical membrane of connecting tubule and collecting duct principal cells. In addition to the apical membrane, Ser269- phosphorylated AQP2 was also detected on the basolateral membrane of connecting tubule cells and inner medullary collecting duct principal cells. OPC-31260 injection following vasopressin stimulation caused internalization of AQP2, a pool of which was phosphorylated at Ser269. These results suggest that 1) AQP2 is phosphorylated at Ser269 intracellularly upon vasopressin stimulation and is rapidly trafficked to the plasma membrane, and 2) AQP2 can be internalized from the plasma membrane even if it remains phosphorylated at Ser269.

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original articles
  • C Deutschmann, B Minnich, A Lametschwandtner
    2017 Volume 77 Issue 1 Pages 1-11
    Published: March 03, 2017
    Released: March 03, 2017

    Summary. In Xenopus laevis Daudin the anlage of the carotid labyrinth, a baro- and chemoreceptor, appears in early premetamorphosis (NF stage 53) as a swelling of the third aortic arch at the point where the common carotid artery gives off the external carotid artery. A conspicuous accumulation of melanocytes preceeds the formation of the labyrinth maze which starts to grow at the end of metamorphic climax (NF stage 64) and continues so through juvenile age. In adult animals the carotid labyrinth displays a spherical to ovoid shape, has an average length of 1.4 mm, a width of about 0.8 mm and a height of about 0.4 mm. The maze vessels form by sprouting angiogenesis from the common carotid artery and the internal carotid artery. Scanning electron microscopy of vascular corrosion casts reveals that size, overall shape, surface morphology and vascular patterns of the carotid labyrinth vary greatly between individuals, whereby intussusceptive microvascular growth (= nonsprouting angiogenesis) and its facets model and contribute to the maturation of the labyrinth’s final vascular patterns. Key words: Xenopus, carotid labyrinth, vascular anatomy, vascular casts, histomorphology

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  • Masato Koike, Ai Kawahara, Masahiro Shibata, Yasuo Uchiyama
    2017 Volume 77 Issue 1 Pages 13-23
    Published: March 03, 2017
    Released: March 03, 2017

    Summary. Neonatal hypoxic/ischemic (H/I) brain injury causes neurological impairment, including cognitive and motor dysfunction as well as seizures. Patterns of H/I injury-induced neuron death using rodent models are considered to be similar to the cases in human H/I encephalopathy. The participation of autophagy in neuron death has been a common feature in neonatal rodent models of H/I brain injury and human H/I encephalopathy when examined by immunochemical approaches for MAP1-LC3. This tendency has also been confirmed in neuronal tissue-specific Atg7 conditional knockout mice. However, while the current rat H/I model that is used for analyzing autophagy results in global damage to the ipsilateral hemisphere, it does not entirely reflect the neuropathological changes that appear in the neonatal mouse H/I model, in which the hippocampus is selectively damaged. The present study established a neonatal rat model of H/I injury with a milder ischemic insult, in which autophagy was involved in the hippocampal CA1 region after H/I injury when examined by electron microscopy, and by immunohistochemical and biochemical analyses of LC3.

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