Match!
Sven Wassmann
Saarland University
83Publications
34H-index
5,565Citations
Publications 83
Newest
Four-and-a-half LIM domain protein-2 (FHL2) is expressed in endothelial and vascular smooth muscle cells. It negatively regulates endothelial cell survival and migration, but its role in atherogenesis is unknown. To investigate the role of FHL2 in atherosclerosis, FHL2-deficient (FHL2-/-) mice were crossed with ApoE-deficient (ApoE -/-) mice, to generate ApoE/FHL2-/- mice. After 7 weeks of high fat diet, ApoE/FHL2-/- mice had significantly smaller (P<0.05) atherosclerotic plaques than ApoE-/- mi...
Abstract Background Endothelial cell recovery requires replenishment of primary cells from the endothelial lineage. However, recent evidence suggests that cells of the innate immune system enhance endothelial regeneration. Methods and results Focusing on mature CD11b + -monocytes, we analyzed the fate and the effect of transfused CD11b + -monocytes after endothelial injury in vivo. CD11b-diphtheria-toxin-receptor-mice – a mouse model in which administration of diphtheria toxin selectively elimin...
#1Talin EbrahimianH-Index: 13
#2Maryam HeidariH-Index: 2
Last.Sven WassmannH-Index: 34
view all 9 authors...
Four-and-a-half LIM domain protein-2 (FHL2) is expressed in vascular cells. FHL2 negatively regulates endothelial cell survival and migration, but its role in atherogenesis is unknown. Methods and ...
OBJECTIVE Four-and-a-half LIM domain protein-2 (FHL2), a member of the FHL family of proteins, is expressed in endothelial and vascular smooth muscle cells. FHL2 negatively regulates endothelial cell survival and migration, but its role in atherogenesis is unknown. METHODS AND RESULTS To investigate the role of FHL2 in atherosclerosis, we crossed FHL2 knockout (FHL2-/-) with apolipoprotein (Apo) E-deficient (ApoE -/-) mice, and fed them a high fat diet for 7 weeks. Despite a total plasma cholest...
#1Vedat TiyeriliH-Index: 9
#2Ulrich M. BecherH-Index: 10
Last.Cornelius MuellerH-Index: 3
view all 7 authors...
Objective Peroxisome-proliferator–activated-receptor-γ (PPARγ) acts as a transcriptional regulator of multiple genes involved in glucose and lipid metabolism. In vitro studies showed that activated PPARγ suppresses AT1R-gene expression and vice versa. However, it has not yet been determined in vivo, whether AT1R-PPARγ-interactions play a relevant role in the pathogenesis of diabetic complications and specifically in accelerated atherosclerosis.
Background: Inhibition of Four-and-a-half LIM domain protein-2 (FHL-2) attenuates atherosclerotic lesion formation and increases endothelial cell migration. Endothelial progenitor cells (EPCs) substantially contribute to endothelial repair. We investigated the role of FHL-2 in the regulation of early outgrowth EPC number and function. Methods and Results: Early outgrowth EPCs were obtained from human peripheral blood. FHL-2 knockdown in EPCs by small-interfering RNA (siRNA) resulted in a signifi...
123456789