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3. Abnormal High-Density Lipoprotein Induces Endothelial Dysfunction via Activation of Toll-like Receptor-2

Author

Speer, Thimoteus, Rohrer, Lucia, Blyszczuk, Przemyslaw, Shroff, Rukshana, Kuschnerus, Kira, Kränkel, Nicolle, Kania, Gabriela, Zewinger, Stephen, Akhmedov, Alexander, Shi, Yi, Martin, Tina, Perisa, Damir, Winnik, Stephan, Müller, Maja F., Sester, Urban, Wernicke, Gabriel, Jung, Andreas, Gutteck, Ursula, Eriksson, Urs, Geisel, Jürgen, Deanfield, John, von Eckardstein, Arnold, Lüscher, Thomas F., Fliser, Danilo, Bahlmann, Ferdinand H., and Landmesser, Ulf

Published
2013
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4. Rapid Inflammasome Activation Is Attenuated in Post-Myocardial Infarction Monocytes

Author

Giral, Hector, primary, Franke, Vedran, additional, Moobed, Minoo, additional, Müller, Maja F., additional, Lübking, Laura, additional, James, Divya Maria, additional, Hartung, Johannes, additional, Kuschnerus, Kira, additional, Meteva, Denitsa, additional, Seppelt, Claudio, additional, Jakob, Philipp, additional, Klingenberg, Roland, additional, Kränkel, Nicolle, additional, Leistner, David, additional, Zeller, Tanja, additional, Blankenberg, Stefan, additional, Zimmermann, Friederike, additional, Haghikia, Arash, additional, Lüscher, Thomas F., additional, Akalin, Altuna, additional, Landmesser, Ulf, additional, and Kratzer, Adelheid, additional

Published
2022
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8. Vascular repair strategies in type 2 diabetes: novel insights

Author

Kuschnerus, Kira, Landmesser, Ulf, and Kränkel, Nicolle

Subjects
Mini-Review
Abstract

Impaired functions of vascular cells are responsible for the majority of complications in patients with type 2 diabetes (T2D). Recently a better understanding of mechanisms contributing to development of vascular dysfunction and the role of systemic inflammatory activation and functional alterations of several secretory organs, of which adipose tissue has more recently been investigated, has been achieved. Notably, the progression of vascular disease within the context of T2D appears to be driven by a multitude of incremental signaling shifts. Hence, successful therapies need to target several mechanisms in parallel, and over a long time period. This review will summarize the latest molecular strategies and translational developments of cardiovascular therapy in patients with T2D.

Published
2015

9. Increased Expression of miR-483-3p Impairs the Vascular Response to Injury in Type 2 Diabetes.

Author

Kuschnerus, Kira, Straessler, Elisabeth T., Müller, Maja F., Lüscher, Thomas F., Landmesser, Ulf, and Kränkel, Nicolle

Subjects
*TYPE 2 diabetes, *ZINC-finger proteins, *WOUNDS & injuries, *TRANSCRIPTION factors
Abstract

Aggravated endothelial injury and impaired endothelial repair capacity contribute to the high cardiovascular risk in patients with type 2 diabetes (T2D), but the underlying mechanisms are still incompletely understood. Here we describe the functional role of a mature form of miRNA (miR) 483-3p, which limits endothelial repair capacity in patients with T2D. Expression of human (hsa)-miR-483-3p was higher in endothelial-supportive M2-type macrophages (M2MΦs) and in the aortic wall of patients with T2D than in control subjects without diabetes. Likewise, the murine (mmu)-miR-483* was higher in T2D than in nondiabetic murine carotid samples. Overexpression of miR-483-3p increased endothelial and macrophage apoptosis and impaired reendothelialization in vitro. The inhibition of hsa-miR-483-3p in human T2D M2MΦs transplanted to athymic nude mice (NMRI-Foxn1ν/Foxn1ν ) or systemic inhibition of mmu-miR-483* in B6.BKS(D)-Leprdb /J diabetic mice rescued diabetes-associated impairment of reendothelialization in the murine carotid-injury model. We identified the endothelial transcription factor vascular endothelial zinc finger 1 (VEZF1) as a direct target of miR-483-3p. VEZF1 expression was reduced in aortae of diabetic mice and upregulated in diabetic murine aortae upon systemic inhibition of mmu-483*. The miRNA miR-483-3p is a critical regulator of endothelial integrity in patients with T2D and may represent a therapeutic target to rescue endothelial regeneration after injury in patients with T2D. [ABSTRACT FROM AUTHOR]

Published
2019
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11. Novel insights into the critical role of bradykinin and the kinin b2 receptor for vascular recruitment of circulating endothelial repair-promoting mononuclear cell subsets: alterations in patients with coronary disease

Author

Kränkel, Nicolle, Kuschnerus, Kira, Müller, Maja, Speer, Timo, Mocharla, Pavani, Madeddu, Paolo, Bader, Michael, Lüscher, Thomas F, Landmesser, Ulf, Kränkel, Nicolle, Kuschnerus, Kira, Müller, Maja, Speer, Timo, Mocharla, Pavani, Madeddu, Paolo, Bader, Michael, Lüscher, Thomas F, and Landmesser, Ulf

Abstract

BACKGROUND: Endothelial injury is considered critical for progression of atherosclerosis and its complications in coronary artery disease (CAD). The endothelial-supportive effects of bradykinin have mainly been attributed to activation of the resident endothelium. Here we newly investigate the role of bradykinin and its B2 receptor for the recruitment and functional activation of circulating mononuclear cell subsets with endothelial-repair promoting capacity, such as CD34(+)CXCR4(+)cells, at sites of arterial injury. METHODS AND RESULTS: Bradykinin-B2-receptor (B2R) blockade by icatibant substantially impaired recruitment of circulating CD34(+)CXCR4(+) mononuclear cells (expressing high levels of B2R) to endothelial cells in vitro and to injured arterial wall in vivo, whereas recruitment of CD14(hi) monocytes (expressing low levels of B2R) was unchanged. Moreover, the capacity of genetically B2R-deficient bone marrow cells to promote endothelial repair in vivo was markedly impaired as compared with wild-type bone marrow cells. B2R expression was reduced on CD34(+)CXCR4(+)mononuclear cells and endothelial repair-promoting early outgrowth cells, but not on CD14(hi)monocytes, from CAD patients as compared with healthy subjects. B2R stimulation induced CD18 activation in early outgrowth cells of healthy subjects, but not in early outgrowth cells of CAD patients. Adenoviral B2R overexpression enhanced in vivo vascular recruitment and rescued impaired endothelial repair capacity of early outgrowth cells from CAD patients. CONCLUSIONS: We newly report that bradykinin/B2R signaling may promote endothelial repair after arterial injury by selective recruitment and functional activation of B2R-expressing circulating mononuclear cell subsets. In CAD patients, B2R downregulation on endothelial repair-promoting circulating mononuclear cells substantially impairs the bradykinin-dependent endothelial repair, representing a novel mechanism promoting endothelial injury in CAD patient

Published
2013

13. Abstract 18317: Abnormal High Density Lipoprotein (HDL) from Patients with Chronic Kidney Disease (CKD) Increases Arterial Blood Pressure: Role of Toll-Like Receptor-2 (TLR-2)

Author

Speer, Timo, primary, Rohrer, Lucia, additional, Blyszczuk, Przemyslaw, additional, Kränkel, Nicolle, additional, Kuschnerus, Kira, additional, Shi, Yi, additional, Akhmedov, Alexander, additional, Zewinger, Stephen, additional, von Eckardstein, Arnold, additional, Lúscher, Thomas, additional, Bahlmann, Ferdinand, additional, Fliser, Danilo, additional, and Landmesser, Ulf, additional

Published
2012
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14. Abstract 16896: Kinin-Mediated Recruitment of Circulating Endothelial Supporting Cells is Impaired in Patients with CAD or Diabetes: Impact on Endothelial Healing

Author

Kraenkel, Nicolle, primary, Kuschnerus, Kira, additional, Mueller, Maja, additional, Speer, Timo, additional, Briand, Sylvie, additional, Bader, Michael, additional, Madeddu, Paolo, additional, Alhenc-Gelas, Francois, additional, Luescher, Thomas F, additional, and Landmesser, Ulf, additional

Published
2011
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15. Vascular repair strategies in type 2 diabetes: novel insights.

Author

Kuschnerus K, Landmesser U, and Kränkel N

Abstract

Impaired functions of vascular cells are responsible for the majority of complications in patients with type 2 diabetes (T2D). Recently a better understanding of mechanisms contributing to development of vascular dysfunction and the role of systemic inflammatory activation and functional alterations of several secretory organs, of which adipose tissue has more recently been investigated, has been achieved. Notably, the progression of vascular disease within the context of T2D appears to be driven by a multitude of incremental signaling shifts. Hence, successful therapies need to target several mechanisms in parallel, and over a long time period. This review will summarize the latest molecular strategies and translational developments of cardiovascular therapy in patients with T2D.

Published
2015
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