Rusan A Catar

Publications of Rusan A Catar

• Aldosterone rapidly induces leukocyte adhesion to endothelial cells: a new link between aldosterone and arteriosclerosis?

  Authors: Alexander W Krug, Steffi Kopprasch, Christian G Ziegler, Sandra Dippong, Rusan A Catar, Stefan R Bornstein, Henning Morawietz, Michael Gekle

  Hypertension. 12/2007; 50(5):e156-7.

• Upregulation of endothelin receptor B in human endothelial cells by low-density lipoproteins.

  Authors: Gregor Muller, Rusan A Catar, Bernd Niemann, Matthias Barton, Lilla Knels, Martina Wendel, Henning Morawietz

  Experimental biology and medicine (Maywood, N.J.). 06/2006; 231(6):766-71.

  Low-density lipoproteins (LDLs) represent the most important treatable risk factors for coronary artery disease. Although it has been previously shown that hypercholesterolemia stimulates theLow-density lipoproteins (LDLs) represent the most important treatable risk factors for coronary artery disease. Although it has been previously shown that hypercholesterolemia stimulates the endothelin system, the effects of increased levels of LDL on endothelial endothelin receptors have not been previously studied. In particular, the influence of native and oxidatively modified LDLs (nLDLs and oxLDLs) and the regulatory mechanisms in endothelial cells are currently unknown. Human endothelial cells almost exclusively express the endothelin receptor type B (ET(B)). Therefore, the effect of nLDL and oxLDL on the expression of ET(B) was studied in primary cultures of human umbilical vein endothelial cells (HUVEC). HUVEC were stimulated by nLDL and oxLDL in a time-dependent (1-12 hrs) and dose-dependent (25-100 microg/ml) manner. To analyze signal transduction pathways involved in the regulation of ET(B), protein kinase C (PKC) was inhibited using 100 nM Ro-31-8220. The mRNA expression of ET(B) was determined by quantitative reverse transcription-polymerase chain reaction and ET(B) protein expression by Western blot. Native LDL induced ET(B) mRNA after 1 hr (100 microg/ml, 199 +/- 35%, n = 15, P < 0.05 vs. control). Stimulation of HUVEC with oxLDL increased ET(B) mRNA expression (1 hr, 100 microg/ml oxLDL: 308 +/- 48%, n = 15, P < 0.05 vs. control) as well. Induction of ET(B) was also found on the protein level. nLDL was even more potent than oxLDL in inducing ET(B) protein expression. Induction of ET(B) expression by oxLDL is mediated by PKC. These data demonstrate that low-density lipoproteins even independent of oxidative modification are potent inducers of ET(B) receptors at the mRNA and protein level in HUVEC. Given the nitric oxide-releasing capacity of endothelial ET(B) receptors, this effect may represent a possible vasoprotective mechanism.

• Novel Nox inhibitor of oxLDL-induced reactive oxygen species formation in human endothelial cells.

  Authors: Claudia Stielow, Rusan A Catar, Gregor Muller, Kirstin Wingler, Peter Scheurer, Harald H H W Schmidt, Henning Morawietz

  Biochemical and biophysical research communications. 05/2006; 344(1):200-5.

  In this study, we investigated effects of a novel NAD(P)H oxidase (Nox)-inhibitor 3-benzyl-7-(2-benzoxazolyl)thio-1,2,3-triazolo[4,5-d]pyrimidine (VAS2870) on oxidized low-density lipoproteinIn this study, we investigated effects of a novel NAD(P)H oxidase (Nox)-inhibitor 3-benzyl-7-(2-benzoxazolyl)thio-1,2,3-triazolo[4,5-d]pyrimidine (VAS2870) on oxidized low-density lipoprotein (oxLDL)-mediated reactive oxygen species (ROS) formation in human endothelial cells. Primary cultures of human umbilical vein endothelial cells were cultured to confluence and ROS formation was induced with 50microg/ml oxLDL for 2h. ROS formation was detected by chemiluminescence (CL) using the Diogenes reagent. OxLDL induced ROS formation in human endothelial cells (171+/-12%; n=10, P<0.05 vs. control). This augmented ROS formation in response to oxLDL was completely inhibited by the Nox inhibitor VAS2870 (101+/-9%; n=7, P<0.05 vs. oxLDL). Similar results were obtained with superoxide dismutase (91+/-7%; n=7, P<0.05 vs. oxLDL). However, the Nox4 mRNA expression level was neither changed by oxLDL nor VAS2870. We conclude that VAS2870 could provide a novel strategy to inhibit the augmented endothelial superoxide anion formation in response to cardiovascular risk factors.

• Native and oxidized low-density lipoproteins stimulate endothelin-converting enzyme-1 expression in human endothelial cells.

  Authors: Bernd Niemann, Susanne Rohrbach, Rusan A Catar, Gregor Muller, Matthias Barton, Henning Morawietz

  Biochemical and biophysical research communications. 10/2005; 334(3):747-53.

  This study addressed the question how different lipoproteins modulate the expression of endothelin-converting enzyme-1 (ECE-1) in human endothelial cells. The effect of native and oxidizedThis study addressed the question how different lipoproteins modulate the expression of endothelin-converting enzyme-1 (ECE-1) in human endothelial cells. The effect of native and oxidized low-density lipoproteins (nLDL, oxLDL) on expression of ECE-1, prepro-endothelin-1, and endothelin-1 peptide was studied in primary cultures of human endothelial cells. Native and oxidized LDL increased ECE-1 mRNA after 1 h, reaching its maximum at 100 microg/ml (1.9- and 2.5-fold, respectively). Furthermore, ECE-1 protein expression, prepro-endothelin-1 mRNA, and endothelin-1 peptide release were increased in response to nLDL or oxLDL. Induction of ECE-1 by nLDL and of prepro-endothelin-1 by oxLDL was reduced by protein kinase C inhibition. Increased expression of ECE-1 mRNA by oxLDL and of prepro-endothelin-1 by nLDL was blocked by an angiotensin II receptor type 1 antagonist. Our data provide evidence for a new mechanism how increased LDL plasma levels might contribute to enhanced endothelin-1 release in patients with hypercholesterolemia.