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1,069 results on '"Schaper, Wolfgang"'

1. Ergänzungsband zu Band 11

Author

Wolfgang Neugebauer, Klaus Neitmann, Uwe Schaper, Wolfgang Neugebauer, Klaus Neitmann, Uwe Schaper

Published
2021

6. Bone Marrow-Derived Cells

Author

Ziegelhoeffer, Tibor, Kostin, Sawa, Fernández, Borja, Heil, Matthias, Schaper, Wolfgang, Schaper, Wolfgang, editor, and Schaper, Jutta, editor

Published
2004
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43. Shear Stress-Induced miR-143-3p in Collateral Arteries Contributes to Outward Vessel Growth by Targeting Collagen V-alpha 2

Author

Troidl, Kerstin, Hammerschick, Thomas, Albarran-Juarez, Julian, Jung, Georg, Schierling, Wilma, Tonack, Sarah, Krueger, Marcus, Matuschke, Benjamin, Troidl, Christian, Schaper, Wolfgang, Schmitz-Rixen, Thomas, Preissner, Klaus T., Fischer, Silvia, Troidl, Kerstin, Hammerschick, Thomas, Albarran-Juarez, Julian, Jung, Georg, Schierling, Wilma, Tonack, Sarah, Krueger, Marcus, Matuschke, Benjamin, Troidl, Christian, Schaper, Wolfgang, Schmitz-Rixen, Thomas, Preissner, Klaus T., and Fischer, Silvia

Abstract

Objective: Arteriogenesis, describing the process of collateral artery growth, is activated by fluid shear stress (FSS). Since this vascular mechanotransduction may involve microRNAs (miRNAs), we investigated the FSS-induced expression of vascular cell miRNAs and their functional impact on collateral artery growth during arteriogenesis. Approach and Results: To this end, rats underwent femoral artery ligation and arteriovenous anastomosis to increase collateral blood flow to maximize FSS and trigger collateral vessel remodeling. Five days after surgery, a miRNA expression profile was obtained from collateral tissue, and upregulation of 4 miRNAs (miR-24-3p, miR-143-3p, miR-146a-5p, and miR-195-5p) was verified by quantitative polymerase chain reaction. Knockdown of miRNAs at the same time of the surgery in an in vivo mouse ligation and recovery model demonstrated that inhibition of miR-143-3p only severely impaired blood flow recovery due to decreased arteriogenesis. In situ hybridization revealed distinct localization of miR-143-3p in the vessel wall of growing collateral arteries predominantly in smooth muscle cells. To investigate the mechanotransduction of FSS leading to the increased miR-143-3p expression, cultured endothelial cells were exposed to FSS. This provoked the expression and release of TGF-beta (transforming growth factor-beta), which increased the expression of miR-143-3p in smooth muscle cells in the presence of SRF (serum response factor) and myocardin. COL5A2 (collagen type V-alpha 2)-a target gene of miR-143-3p predicted by in silico analysis-was found to be downregulated in growing collaterals. Conclusions: These results indicate that the increased miR-143-3p expression in response to FSS might contribute to the reorganization of the extracellular matrix, which is important for vascular remodeling processes, by inhibiting collagen V-alpha 2 biosynthesis.

Published
2020

44. The lipopeptide MALP-2 promotes collateral growth

Author

Troidl, Kerstin, Schubert, Christian, Vlacil, Ann-Kathrin, Chennupati, Ramesh, Koch, Sören, Schütt, Jutta, Oberoi, Raghav, Schaper, Wolfgang, Schmitz-Rixen, Thomas, Schieffer, Bernhard, Grote, Karsten, Troidl, Kerstin, Schubert, Christian, Vlacil, Ann-Kathrin, Chennupati, Ramesh, Koch, Sören, Schütt, Jutta, Oberoi, Raghav, Schaper, Wolfgang, Schmitz-Rixen, Thomas, Schieffer, Bernhard, and Grote, Karsten

Abstract

Beyond their role in pathogen recognition and the initiation of immune defense, Toll-like receptors (TLRs) are known to be involved in various vascular processes in health and disease. We investigated the potential of the lipopeptide and TLR2/6 ligand macrophage activating protein of 2-kDA (MALP-2) to promote blood flow recovery in mice. Hypercholesterolemic apolipoprotein E (Apoe)-deficient mice were subjected to microsurgical ligation of the femoral artery. MALP-2 significantly improved blood flow recovery at early time points (three and seven days), as assessed by repeated laser speckle imaging, and increased the growth of pre-existing collateral arteries in the upper hind limb, along with intimal endothelial cell proliferation in the collateral wall and pericollateral macrophage accumulation. In addition, MALP-2 increased capillary density in the lower hind limb. MALP-2 enhanced endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) release from endothelial cells and improved the experimental vasorelaxation of mesenteric arteries ex vivo. In vitro, MALP-2 led to the up-regulated expression of major endothelial adhesion molecules as well as their leukocyte integrin receptors and consequently enhanced the endothelial adhesion of leukocytes. Using the experimental approach of femoral artery ligation (FAL), we achieved promising results with MALP-2 to promote peripheral blood flow recovery by collateral artery growth.

Published
2020

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