Universität zu Köln

Pryymachuk, Galyna, El-Awaad, Ehab ORCID: 0000-0003-3383-6384, Piekarek, Nadin, Drebber, Uta, Maul, Alexandra C., Hescheler, Juergen, Wodarz, Andreas ORCID: 0000-0002-0007-6289, Pfitzer, Gabriele, Neiss, Wolfram F., Pietsch, Markus ORCID: 0000-0002-8110-2265 and Schroeter, Mechthild M. (2022). Angiotensin II type 1 receptor localizes at the blood-bile barrier in humans and pigs. Histochem. Cell Biol., 157 (5). S. 513 - 525. NEW YORK: SPRINGER. ISSN 1432-119X

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Abstract

Animal models and clinical studies suggest an influence of angiotensin II (AngII) on the pathogenesis of liver diseases via the renin-angiotensin system. AngII application increases portal blood pressure, reduces bile flow, and increases permeability of liver tight junctions. Establishing the subcellular localization of angiotensin II receptor type 1 (AT1R), the main AngII receptor, helps to understand the effects of AngII on the liver. We localized AT1R in situ in human and porcine liver and porcine gallbladder by immunohistochemistry. In order to do so, we characterized commercial anti-AT1R antibodies regarding their capability to recognize heterologous human AT1R in immunocytochemistry and on western blots, and to detect AT1R using overlap studies and AT1R-specific blocking peptides. In hepatocytes and canals of Hering, AT1R displayed a tram-track-like distribution, while in cholangiocytes AT1R appeared in a honeycomb-like pattern; i.e., in liver epithelia, AT1R showed an equivalent distribution to that in the apical junctional network, which seals bile canaliculi and bile ducts along the blood-bile barrier. In intrahepatic blood vessels, AT1R was most prominent in the tunica media. We confirmed AT1R localization in situ to the plasma membrane domain, particularly between tight and adherens junctions in both human and porcine hepatocytes, cholangiocytes, and gallbladder epithelial cells using different anti-AT1R antibodies. Localization of AT1R at the junctional complex could explain previously reported AngII effects and predestines AT1R as a transmitter of tight junction permeability.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Pryymachuk, Galyna UNSPECIFIED UNSPECIFIED UNSPECIFIED El-Awaad, Ehab UNSPECIFIED orcid.org/0000-0003-3383-6384 UNSPECIFIED Piekarek, Nadin UNSPECIFIED UNSPECIFIED UNSPECIFIED Drebber, Uta UNSPECIFIED UNSPECIFIED UNSPECIFIED Maul, Alexandra C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Hescheler, Juergen UNSPECIFIED UNSPECIFIED UNSPECIFIED Wodarz, Andreas UNSPECIFIED orcid.org/0000-0002-0007-6289 UNSPECIFIED Pfitzer, Gabriele UNSPECIFIED UNSPECIFIED UNSPECIFIED Neiss, Wolfram F. UNSPECIFIED UNSPECIFIED UNSPECIFIED Pietsch, Markus UNSPECIFIED orcid.org/0000-0002-8110-2265 UNSPECIFIED Schroeter, Mechthild M. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-673445
DOI:	10.1007/s00418-022-02087-z
Journal or Publication Title:	Histochem. Cell Biol.
Volume:	157
Number:	5
Page Range:	S. 513 - 525
Date:	2022
Publisher:	SPRINGER
Place of Publication:	NEW YORK
ISSN:	1432-119X
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language IMMUNOHISTOCHEMICAL LOCALIZATION; AT(1) RECEPTORS; HUMAN-LIVER; SYSTEM; PROTEIN; EXPRESSION; CELLS; ACTIVATION; ORGANIZATION; CONTRACTION Multiple languages Cell Biology; Microscopy Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/67344