W
Wolfgang Erl
Researcher at Ludwig Maximilian University of Munich
Publications - 45
Citations - 4677
Wolfgang Erl is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Endothelial stem cell & Cell adhesion molecule. The author has an hindex of 28, co-authored 45 publications receiving 4515 citations. Previous affiliations of Wolfgang Erl include Brigham and Women's Hospital & Karolinska Institutet.
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Endothelial Progenitor Cells Mobilization, Differentiation, and Homing
TL;DR: Clinical studies using EPCs for neovascularization have just been started; however, the mechanisms stimulating or inhibiting the differentiation of EPC in vivo and the signals causing their migration and homing to sites of injured endothelium or extravascular tissue are largely unknown at present.
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HMG-CoA Reductase Inhibitors Decrease CD11b Expression and CD11b-Dependent Adhesion of Monocytes to Endothelium and Reduce Increased Adhesiveness of Monocytes Isolated From Patients With Hypercholesterolemia
TL;DR: The reduction ofCD11b expression and inhibition of CD11b-dependent monocyte adhesion to endothelium may crucially contribute to the clinical benefit of HMG-CoA reductase inhibitors in CHD, independent of cholesterol-lowering effects.
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Apoptotic bodies from endothelial cells enhance the number and initiate the differentiation of human endothelial progenitor cells in vitro.
TL;DR: The results suggest that apoptotic bodies from ECs are taken up by EPCs, increasing their number and differentiation state and may represent a new signaling pathway between progenitor and damaged somatic cells.
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Antioxidants inhibit monocyte adhesion by suppressing nuclear factor-kappa B mobilization and induction of vascular cell adhesion molecule-1 in endothelial cells stimulated to generate radicals.
Christian Weber,Wolfgang Erl,Angelika Pietsch,M Strobel,H W Ziegler-Heitbrock,Peter C. Weber +5 more
TL;DR: Although ICAM-1 induction was unaffected, inhibitors of NADPH oxidase (apocynin) or cytochrome P-450 (SKF525a) suppressed VCAM- 1 induction by TNF, revealing that several radical-generating systems are involved in its regulation.
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Aspirin Inhibits Nuclear Factor–κB Mobilization and Monocyte Adhesion in Stimulated Human Endothelial Cells
TL;DR: It is suggested that aspirin inhibits NF-kappa B mobilization, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin.