Journalartikel
Autorenliste: Guenduez, Dursun; Aslam, Muhammad; Krieger, Uwe; Becker, Lutz; Grebe, Mathias; Arshad, Muhammad; Sedding, Daniel G.; Haertel, Frauke V.; Abdallah, Yaser; Piper, Hans Michael; Voss, Reinhard K.; Noll, Thomas
Jahr der Veröffentlichung: 2012
Seiten: 962-970
Zeitschrift: Journal of Molecular and Cellular Cardiology
Bandnummer: 52
Heftnummer: 5
ISSN: 0022-2828
eISSN: 1095-8584
DOI Link: https://doi.org/10.1016/j.yjmcc.2012.01.003
Verlag: Elsevier
Abstract:
ATP can differentially affect the micro- and macrovascular endothelial barrier. It has been shown that it can both increase and/or decrease macromolecule permeability of microvascular endothelial cells and microvessels, in vivo. We hypothesised that the barrier stabilising effect is mediated by ATP itself via P2 receptors, while barrier-disrupting effect is mediated by its metabolite adenosine via adenosine receptors. The effects of ATP, ADP, AMP and adenosine on barrier function were studied in cultured rat coronary microvascular endothelial monolayers (RCEC) in vitro, as well as in rat mesentery vessels, and in rat hearts in vivo. ATP and ADP showed a biphasic effect on permeability of RCEC monolayers with a reduction followed by a later increase in albumin permeability. The permeability decreasing effect of ATP was enhanced by ectonucleotidase inhibitor ARL67156 while permeability increasing effect was enhanced by apyrase, an extracellular ecto-nucleotidase. Moreover, the permeability increasing effect was abrogated by adenosine receptor antagonists, 8-phenyltheophylline (8-PT) and DMPX. Adenosine and adenosine receptor agonists 5'-(N-ethylcarboxamido)-adenosine (NECA), CGS21680, and R-PIA enhanced albumin permeability which was antagonised by 8-PT, A(1), and A(2) but not by A(3) receptor antagonists. Likewise, immunofluorescence microscopy of VE-cadherin and actin showed that NECA induces a disturbance of intercellular junctions. Preincubation of ATP antagonised the effects of NECA on permeability, actin cytoskeleton and intercellular junctions. Similar effects of the applied substances were observed in rat mesentery artery by determining the vascular leakage using intravital microscopy as well as in rat hearts by assessing myocardial water contents in vivo. In conclusion, the study demonstrates that in RCEC, ATP, ADP, and its metabolite adenosine play opposing roles on endothelial barrier function. (C) 2012 Elsevier Ltd. All rights reserved.
Zitierstile
Harvard-Zitierstil: Guenduez, D., Aslam, M., Krieger, U., Becker, L., Grebe, M., Arshad, M., et al. (2012) Opposing effects of ATP and adenosine on barrier function of rat coronary microvasculature, Journal of Molecular and Cellular Cardiology, 52(5), pp. 962-970. https://doi.org/10.1016/j.yjmcc.2012.01.003
APA-Zitierstil: Guenduez, D., Aslam, M., Krieger, U., Becker, L., Grebe, M., Arshad, M., Sedding, D., Haertel, F., Abdallah, Y., Piper, H., Voss, R., & Noll, T. (2012). Opposing effects of ATP and adenosine on barrier function of rat coronary microvasculature. Journal of Molecular and Cellular Cardiology. 52(5), 962-970. https://doi.org/10.1016/j.yjmcc.2012.01.003
Schlagwörter
acute lung injury; Adenosine 5 '-triphosphate; Adenosine receptors; Cadherin; EXTRACELLULAR ATP; GLYCOCALYX; Intravital microscopy; MACROMOLECULE PERMEABILITY; P2-PURINERGIC RECEPTORS; Paracellular permeability; REPERFUSION INJURY; TRIPHOSPHATE