Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Katrin Kliche"'
Publikováno v:
Cellular Physiology and Biochemistry, Vol 35, Iss 3, Pp 1107-1115 (2015)
Background: Similar as in vascular endothelium the negatively charged glycocalyx of erythrocytes selectively buffers sodium. Loss of glycocalyx (i.e. loss of negative charges) leads to increased erythrocyte sodium sensitivity (ESS) quantified by a re
Externí odkaz:
https://doaj.org/article/d0d40e32125c4a2890a6f41ad09efb91
Publikováno v:
Cellular Physiology and Biochemistry, Vol 35, Iss 3, Pp 1107-1115 (2015)
Background: Similar as in vascular endothelium the negatively charged glycocalyx of erythrocytes selectively buffers sodium. Loss of glycocalyx (i.e. loss of negative charges) leads to increased erythrocyte sodium sensitivity (ESS) quantified by a re
Autor:
Hans Oberleithner, Verena Drüppel, Katrin Kliche, Moritz Paar, Hermann Pavenstädt, Kristina Kusche-Vihrog
Publikováno v:
Hypertension. 64:391-396
The epithelial sodium channel is also expressed in vascular endothelium (endothelial sodium channel [EnNaC]). Depending on ambient sodium concentration, EnNaC is associated with mechanical stiffening of the endothelial cell cortex, leading to endothe
Autor:
Verena Drüppel, Katrin Kliche, Hans Oberleithner, Kristina Kusche-Vihrog, Bernd Kasprzak, Hermann Pavenstädt, Claudia Grossmann, Michael Gekle, Eva Brand
Publikováno v:
The FASEB Journal. 27:3652-3659
Aldosterone triggers the stiff endothelial cell syndrome (SECS), characterized by an up-regulation of epithelial sodium channels (ENaCs) and mechanical stiffening of the endothelial cell cortex accompanied by endothelial dysfunction. In vivo, aldoste
Autor:
Katrin Kliche, Hans Oberleithner, Kilian Oberleithner, Stefanie Korte, Kristina Kusche-Vihrog, Wladimir Peters, Hermann Schillers
Publikováno v:
Pflugers Archiv
Sodium overload stiffens vascular endothelial cells in vitro and promotes arterial hypertension in vivo. The hypothesis was tested that the endothelial glycocalyx (eGC), a mesh of anionic biopolymers covering the surface of the endothelium, participa
Autor:
Ivan Liashkovich, Katrin Kliche, Chiara Callies, Kristina Kusche-Vihrog, Johannes Fels, Hans Oberleithner, Pia Jeggle
Publikováno v:
Journal of Cell Science. 124:1936-1942
The stiffness of vascular endothelial cells is crucial to mechanically withstand blood flow and, at the same time, to control deformation-dependent nitric oxide release. However, the regulation of mechanical stiffness is not yet understood. There is
Publikováno v:
Pflügers Archiv - European Journal of Physiology. 462:209-217
The vascular endothelium plays a crucial role in vessel homeostasis and is implicated in the pathogenesis of cardiovascular disease. The function and life span of endothelial cells, therefore, have a large impact upon the quality and expectancy of an
Autor:
Uta Hillebrand, Katrin Kliche, Detlef Lang, Hans Oberleithner, Christian Stock, Claudia Hagedorn, Stefan Reuter, Hermann Pavenstädt, Ralph Telgmann, Martin Hausberg, Eckhart Büssemaker
Publikováno v:
Journal of Hypertension. 27:517-526
Nebivolol (NEB) is a [beta]1-receptor blocker with nitric oxide-dependent vasodilating properties. NEB-induced nitric oxide release is mediated through the estrogen receptor.Here, we tested the hypothesis that NEB decreases endothelial cell stiffness
Autor:
Eva Brand, Anja Blanque, Katrin Kliche, Hermann Schillers, Katarina Urbanova, Hans Oberleithner, Marianne Wilhelmi, Kristina Kusche-Vihrog, Hermann Pavenstädt
Publikováno v:
Hypertension (Dallas, Tex. : 1979). 57(2)
Elevation of C-reactive protein (CRP) in human blood accompanies inflammatory processes, including cardiovascular diseases. There is increasing evidence that the acute-phase reactant CRP is not only a passive marker protein for systemic inflammation
Autor:
Uta Hillebrand, Christian Stock, Yvonne Ludwig, Michaela Kuhn, Katrin Kliche, Hans Oberleithner
Publikováno v:
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 18(4-5)
There is growing evidence that aldosterone acts on heart where it causes cellular remodeling and hypertrophy. Since it is still unclear whether aldosterone directly acts on cardiomyocytes or indirectly, by an altered electrolyte balance in the organi