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16 results on '"Wu, Xuekun"'

2. Myeloid-Derived Growth Factor Protects Against Pressure Overload–Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca2+-ATPase Expression in Cardiomyocytes

Author

Korf-Klingebiel, Mortimer, Reboll, Marc R., Polten, Felix, Weber, Natalie, Jäckle, Felix, Wu, Xuekun, Kallikourdis, Marinos, Kunderfranco, Paolo, Condorelli, Gianluigi, Giannitsis, Evangelos, Kustikova, Olga S., Schambach, Axel, Pich, Andreas, Widder, Julian D., Bauersachs, Johann, van den Heuvel, Joop, Kraft, Theresia, Wang, Yong, and Wollert, Kai C.

Published
2021
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10. Meteorin-like promotes heart repair through endothelial KIT receptor tyrosine kinase

Author

Reboll, Marc R., primary, Klede, Stefanie, additional, Taft, Manuel H., additional, Cai, Chen-Leng, additional, Field, Loren J., additional, Lavine, Kory J., additional, Koenig, Andrew L., additional, Fleischauer, Jenni, additional, Meyer, Johann, additional, Schambach, Axel, additional, Niessen, Hans W., additional, Kosanke, Maike, additional, van den Heuvel, Joop, additional, Pich, Andreas, additional, Bauersachs, Johann, additional, Wu, Xuekun, additional, Zheng, Linqun, additional, Wang, Yong, additional, Korf-Klingebiel, Mortimer, additional, Polten, Felix, additional, and Wollert, Kai C., additional

Published
2022
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11. Myeloid-Derived Growth Factor Protects Against Pressure Overload–Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca 2+ -ATPase Expression in Cardiomyocytes

Author

Korf-Klingebiel, Mortimer, primary, Reboll, Marc R., additional, Polten, Felix, additional, Weber, Natalie, additional, Jäckle, Felix, additional, Wu, Xuekun, additional, Kallikourdis, Marinos, additional, Kunderfranco, Paolo, additional, Condorelli, Gianluigi, additional, Giannitsis, Evangelos, additional, Kustikova, Olga S., additional, Schambach, Axel, additional, Pich, Andreas, additional, Widder, Julian D., additional, Bauersachs, Johann, additional, van den Heuvel, Joop, additional, Kraft, Theresia, additional, Wang, Yong, additional, and Wollert, Kai C., additional

Published
2021
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14. Heparan Sulfate-Editing Extracellular Sulfatases Enhance Vascular Endothelial Growth Factor Bioavailability for Ischemic Heart Repair

Author

Korf-Klingebiel, Mortimer, Reboll, Marc R, Grote, Karsten, Schleiner, Hauke, Wang, Yong, Wu, Xuekun, Klede, Stefanie, Mikhed, Yuliya, Bauersachs, Johann, Klintschar, Michael, Rudat, Carsten, Kispert, Andreas, Niessen, Hans Wm, Lübke, Torben, Dierks, Thomas, and Wollert, Kai C

Abstract

RATIONALE: Mechanistic insight into the inflammatory response after acute myocardial infarction (MI) may inform new molecularly-targeted treatment strategies to prevent chronic heart failure.; OBJECTIVE: We identified the sulfatase SULF2 in an in silico secretome analysis in bone marrow cells from patients with acute MI and detected increased sulfatase activity in myocardial autopsy samples. SULF2 (Sulf2 in mice) and its isoform SULF1 (Sulf1) act as endo-sulfatases removing 6 O sulfate groups from heparan sulfate (HS) in the extracellular space, thus eliminating docking sites for HS binding proteins. We hypothesized that the Sulfs have a role in tissue repair after MI.; METHODS AND RESULTS: Both Sulfs were dynamically upregulated after coronary artery ligation in mice, attaining peak expression and activity levels during the first week after injury. Sulf2 was expressed by monocytes and macrophages, Sulf1 by endothelial cells and fibroblasts. Infarct border-zone capillarization was impaired, scar size increased, and cardiac dysfunction more pronounced in mice with a genetic deletion of either Sulf1 or Sulf2. Studies in bone marrow-chimeric Sulf-deficient mice and Sulf-deficient cardiac endothelial cells established that inflammatory cell-derived Sulf2 and endothelial cell-autonomous Sulf1 promote angiogenesis. Mechanistically, both Sulfs reduced HS sulfation in the infarcted myocardium, thereby diminishing vascular endothelial growth factor A (Vegfa) interaction with HS. Along this line, both Sulfs rendered infarcted mouse heart explants responsive to the angiogenic effects of HS-binding Vegfa164 but did not modulate the angiogenic effects of non-HS-binding Vegfa120. Treating wild-type mice systemically with the small molecule HS antagonist surfen (bis 2 methyl-4-amino-quinolyl-6-carbamide, 1 mg/kg/day) for 7 days after MI released Vegfa from HS, enhanced infarct border-zone capillarization, and exerted sustained beneficial effects on cardiac function and survival.; CONCLUSIONS: These findings establish HS-editing Sulfs as critical inducers of postinfarction angiogenesis and identify HS sulfation as a therapeutic target for ischemic tissue repair.

Published
2019

15. Angiogenesis after acute myocardial infarction.

Author

Wu, Xuekun, Reboll, Marc R, Korf-Klingebiel, Mortimer, and Wollert, Kai C

Subjects
*MYOCARDIAL infarction, *FATE mapping (Genetics), *NEOVASCULARIZATION, *CARDIOVASCULAR diseases risk factors, *CELL populations, *CELL communication
Abstract

Acute myocardial infarction (MI) inflicts massive injury to the coronary microcirculation leading to vascular disintegration and capillary rarefication in the infarct region. Tissue repair after MI involves a robust angiogenic response that commences in the infarct border zone and extends into the necrotic infarct core. Technological advances in several areas have provided novel mechanistic understanding of postinfarction angiogenesis and how it may be targeted to improve heart function after MI. Cell lineage tracing studies indicate that new capillary structures arise by sprouting angiogenesis from pre-existing endothelial cells (ECs) in the infarct border zone with no meaningful contribution from non-EC sources. Single-cell RNA sequencing shows that ECs in infarcted hearts may be grouped into clusters with distinct gene expression signatures, likely reflecting functionally distinct cell populations. EC-specific multicolour lineage tracing reveals that EC subsets clonally expand after MI. Expanding EC clones may arise from tissue-resident ECs with stem cell characteristics that have been identified in multiple organs including the heart. Tissue repair after MI involves interactions among multiple cell types which occur, to a large extent, through secreted proteins and their cognate receptors. While we are only beginning to understand the full complexity of this intercellular communication, macrophage and fibroblast populations have emerged as major drivers of the angiogenic response after MI. Animal data support the view that the endogenous angiogenic response after MI can be boosted to reduce scarring and adverse left ventricular remodelling. The improved mechanistic understanding of infarct angiogenesis therefore creates multiple therapeutic opportunities. During preclinical development, all proangiogenic strategies should be tested in animal models that replicate both cardiovascular risk factor(s) and the pharmacotherapy typically prescribed to patients with acute MI. Considering that the majority of patients nowadays do well after MI, clinical translation will require careful selection of patients in need of proangiogenic therapies. [ABSTRACT FROM AUTHOR]

Published
2021
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16. Abstract 293: Effect of Cardiovascular Health and Text Messaging (CHAT) on Risk Factor Management in Patients with Coronary Heart Disease: A Randomized Clinical Trial

Author

Zheng, Xin, primary, Spatz, Erica S, additional, Bai, Xueke, additional, Huo, Xiqian, additional, Ding, Qinglan, additional, Horak, Paul, additional, Wu, Xuekun, additional, Guan, Wenchi, additional, Chow, Clara K, additional, Yan, Xiaofang, additional, Sun, Ying, additional, Wang, Xiuling, additional, Zhang, Haibo, additional, Liu, Jiamin, additional, Li, Jing, additional, Li, Xi, additional, Spertus, John A, additional, Masoudi, Frederick A, additional, and Krumholz, Harlan M, additional

Published
2019
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