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Book ; Thesis: ADAM proteases as therapeutic target in pulmonary and vascular diseases

Yildiz, Daniela

2019

Author's details	vorgelegt von Dr. rer. nat. Daniela Yildiz geb. Dreymüller
Language	English
Size	1 Band (verschiedene Zählungen), Illustrationen, Diagramme
Publishing place	Aachen
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Habilitationsschrift, Rheinisch-Westfälische Technische Hochschule Aachen, 2019
Note	Die Habilitationsschrift besteht aus einem Text und 5 Aufsätzen, die zuvor in verschiedenen Publikationen veröffentlicht wurden
HBZ-ID	HT020151286
Database	Catalogue ZB MED Medicine, Health

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2019 E 1017	order for loan	Magazin

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Article ; Online: Considerations on inhibition approaches for proinflammatory functions of ADAM proteases.

Dreymueller, Daniela / Ludwig, Andreas

Platelets

2017 Volume 28, Issue 4, Page(s) 354–361

Abstract: Proteases of the disintegrin and metalloproteinase (ADAM) family mediate the proteolytic shedding of various surface molecules including cytokine precursors, adhesion molecules, growth factors, and receptors. Within the vasculature ADAM10 and ADAM17 ... ...

Abstract	Proteases of the disintegrin and metalloproteinase (ADAM) family mediate the proteolytic shedding of various surface molecules including cytokine precursors, adhesion molecules, growth factors, and receptors. Within the vasculature ADAM10 and ADAM17 regulate endothelial permeability, transendothelial leukocyte migration, and the adhesion of leukocytes and platelets. In vivo studies show that both proteases are implicated in several inflammatory pathologies, for example, edema formation, leukocyte infiltration, and thrombosis. However, both proteases also contribute to developmental and regenerative processes. Thus, although ADAMs can be regarded as valuable drug targets in many aspects, the danger of severe side effects is clearly visible. To circumvent these side effects, traditional inhibition approaches have to be improved to target ADAMs at the right time in the right place. Moreover, the inhibitors need to be more selective for the target protease and if possible also for the substrate. Antibodies recognizing the active conformation of ADAMs or small molecules blocking exosites of ADAM proteases may represent inhibitors with the desired selectivities.
Language	English
Publishing date	2017-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1034283-7
ISSN	1369-1635 ; 0953-7104
ISSN (online)	1369-1635
ISSN	0953-7104
DOI	10.1080/09537104.2016.1203396
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Article ; Online: Shear Stress Counteracts Endothelial CX3CL1 Induction and Monocytic Cell Adhesion.

Babendreyer, Aaron / Molls, Lisa / Dreymueller, Daniela / Uhlig, Stefan / Ludwig, Andreas

Mediators of inflammation

2017 Volume 2017, Page(s) 1515389

Abstract: Flow conditions critically regulate endothelial cell functions in the vasculature. Reduced shear stress resulting from disturbed blood flow can drive the development of vascular inflammatory lesions. On endothelial cells, the transmembrane chemokine ... ...

Abstract	Flow conditions critically regulate endothelial cell functions in the vasculature. Reduced shear stress resulting from disturbed blood flow can drive the development of vascular inflammatory lesions. On endothelial cells, the transmembrane chemokine CX3CL1/fractalkine promotes vascular inflammation by functioning as a surface-expressed adhesion molecule and by becoming released as soluble chemoattractant for monocytic cells expressing the receptor CX3CR1. Here, we report that endothelial cells from human artery, vein, or microvasculature constitutively express CX3CL1 when cultured under static conditions. Stimulation with TNF
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2017/1515389
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Article ; Online: ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.

Dreymueller, Daniela / Uhlig, Stefan / Ludwig, Andreas

American journal of physiology. Lung cellular and molecular physiology

2014 Volume 308, Issue 4, Page(s) L325–43

Abstract: Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and ... ...

Abstract	Acute and chronic lung inflammation is driven and controlled by several endogenous mediators that undergo proteolytic conversion from surface-expressed proteins to soluble variants by a disintegrin and metalloproteinase (ADAM)-family members. TNF and epidermal growth factor receptor ligands are just some of the many substrates by which these proteases regulate inflammatory or regenerative processes in the lung. ADAM10 and ADAM17 are the most prominent members of this protease family. They are constitutively expressed in most lung cells and, as recent research has shown, are the pivotal shedding enzymes mediating acute lung inflammation in a cell-specific manner. ADAM17 promotes endothelial and epithelial permeability, transendothelial leukocyte migration, and inflammatory mediator production by smooth muscle and epithelial cells. ADAM10 is critical for leukocyte migration and alveolar leukocyte recruitment. ADAM10 also promotes allergic asthma by driving B cell responses. Additionally, ADAM10 acts as a receptor for Staphylococcus aureus (S. aureus) α-toxin and is crucial for bacterial virulence. ADAM8, ADAM9, ADAM15, and ADAM33 are upregulated during acute or chronic lung inflammation, and recent functional or genetic analyses have linked them to disease development. Pharmacological inhibitors that allow us to locally or systemically target and differentiate ADAM-family members in the lung suppress acute and asthmatic inflammatory responses and S. aureus virulence. These promising results encourage further research to develop therapeutic strategies based on selected ADAMs. These studies need also to address the role of the ADAMs in repair and regeneration in the lung to identify further therapeutic opportunities and possible side effects.
MeSH term(s)	ADAM Proteins/metabolism ; Animals ; Asthma/metabolism ; Asthma/pathology ; B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Bacterial Toxins/metabolism ; Epidermal Growth Factor/metabolism ; Gene Expression Regulation, Enzymologic ; Hemolysin Proteins/metabolism ; Humans ; Pneumonia, Staphylococcal/metabolism ; Pneumonia, Staphylococcal/pathology ; Proteolysis ; Staphylococcal Infections ; Staphylococcus aureus/pathogenicity ; Transendothelial and Transepithelial Migration ; Tumor Necrosis Factor-alpha/metabolism ; Virulence Factors/metabolism
Chemical Substances	Bacterial Toxins ; Hemolysin Proteins ; TNF protein, human ; Tumor Necrosis Factor-alpha ; Virulence Factors ; staphylococcal alpha-toxin ; Epidermal Growth Factor (62229-50-9) ; ADAM Proteins (EC 3.4.24.-)
Language	English
Publishing date	2014-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00294.2014
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Article: The role of ADAM-mediated shedding in vascular biology

Dreymueller, Daniela / Pruessmeyer, Jessica / Groth, Ester / Ludwig, Andreas

European journal of cell biology. 2012 , v. 91, no. 6-7

2012

Abstract: Within the vasculature the disintegrins and metalloproteinases (ADAMs) 8, 9, 10, 12, 15, 17, 19, 28 and 33 are expressed on endothelial cells, smooth muscle cells and on leukocytes. As surface-expressed proteases they mediate cleavage of vascular surface ...

Abstract	Within the vasculature the disintegrins and metalloproteinases (ADAMs) 8, 9, 10, 12, 15, 17, 19, 28 and 33 are expressed on endothelial cells, smooth muscle cells and on leukocytes. As surface-expressed proteases they mediate cleavage of vascular surface molecules at an extracellular site close to the membrane. This process is termed shedding and leads to the release of a soluble substrate ectodomain thereby critically modulating the biological function of the substrate. In the vasculature several surface molecules undergo ADAM-mediated shedding including tumour necrosis factor (TNF) α, interleukin (IL) 6 receptor α, L-selectin, vascular endothelial (VE)-cadherin, the transmembrane CX3C-chemokine ligand (CX3CL) 1, Notch, transforming growth factor (TGF) and heparin-binding epidermal growth factor (HB-EGF). These substrates play distinct roles in vascular biology by promoting inflammation, permeability changes, leukocyte recruitment, resolution of inflammation, regeneration and/or neovascularisation. Especially ADAM17 and ADAM10 are capable of cleaving many substrates with diverse function within the vasculature, whereas other ADAMs have a more restricted substrate range. Therefore, targeting ADAM17 or ADAM10 by pharmacologic inhibition or gene knockout not only attenuates the inflammatory response in animal models but also affects tissue regeneration and neovascularisation. Recent discoveries indicate that other ADAMs (e.g. ADAM8 and 9) also play important roles in vascular biology but appear to have more selective effects on vascular responses (e.g. on neovascularisation only). Although, targeting of ADAM17 and ADAM10 in inflammatory diseases is still a promising approach, temporal and spatial as well as substrate-specific inhibition approaches are required to minimise undesired side effects on vascular cells.
Keywords	adverse effects ; animal models ; endothelial cells ; epidermal growth factor ; gene targeting ; inflammation ; interleukins ; leukocytes ; metalloproteinases ; myocytes ; permeability ; smooth muscle ; tissue repair ; transforming growth factors
Language	English
Dates of publication	2012-06
Size	p. 472-485.
Publishing place	Elsevier GmbH
Document type	Article
ZDB-ID	391967-5
ISSN	1618-1298 ; 0070-2463 ; 0171-9335
ISSN (online)	1618-1298
ISSN	0070-2463 ; 0171-9335
DOI	10.1016/j.ejcb.2011.09.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The role of ADAM-mediated shedding in vascular biology.

Dreymueller, Daniela / Pruessmeyer, Jessica / Groth, Ester / Ludwig, Andreas

European journal of cell biology

2012 Volume 91, Issue 6-7, Page(s) 472–485

Abstract	Within the vasculature the disintegrins and metalloproteinases (ADAMs) 8, 9, 10, 12, 15, 17, 19, 28 and 33 are expressed on endothelial cells, smooth muscle cells and on leukocytes. As surface-expressed proteases they mediate cleavage of vascular surface molecules at an extracellular site close to the membrane. This process is termed shedding and leads to the release of a soluble substrate ectodomain thereby critically modulating the biological function of the substrate. In the vasculature several surface molecules undergo ADAM-mediated shedding including tumour necrosis factor (TNF) α, interleukin (IL) 6 receptor α, L-selectin, vascular endothelial (VE)-cadherin, the transmembrane CX3C-chemokine ligand (CX3CL) 1, Notch, transforming growth factor (TGF) and heparin-binding epidermal growth factor (HB-EGF). These substrates play distinct roles in vascular biology by promoting inflammation, permeability changes, leukocyte recruitment, resolution of inflammation, regeneration and/or neovascularisation. Especially ADAM17 and ADAM10 are capable of cleaving many substrates with diverse function within the vasculature, whereas other ADAMs have a more restricted substrate range. Therefore, targeting ADAM17 or ADAM10 by pharmacologic inhibition or gene knockout not only attenuates the inflammatory response in animal models but also affects tissue regeneration and neovascularisation. Recent discoveries indicate that other ADAMs (e.g. ADAM8 and 9) also play important roles in vascular biology but appear to have more selective effects on vascular responses (e.g. on neovascularisation only). Although, targeting of ADAM17 and ADAM10 in inflammatory diseases is still a promising approach, temporal and spatial as well as substrate-specific inhibition approaches are required to minimise undesired side effects on vascular cells.
MeSH term(s)	ADAM Proteins/genetics ; ADAM Proteins/metabolism ; Animals ; Cells, Cultured ; Gene Expression Regulation, Enzymologic ; Humans ; Vascular Diseases/enzymology
Chemical Substances	ADAM Proteins (EC 3.4.24.-)
Language	English
Publishing date	2012-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391967-5
ISSN	1618-1298 ; 0070-2463 ; 0171-9335
ISSN (online)	1618-1298
ISSN	0070-2463 ; 0171-9335
DOI	10.1016/j.ejcb.2011.09.003
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Article ; Online: The perioperative time course and clinical significance of the chemokine CXCL16 in patients undergoing cardiac surgery.

Dreymueller, Daniela / Goetzenich, Andreas / Emontzpohl, Christoph / Soppert, Josefin / Ludwig, Andreas / Stoppe, Christian

Journal of cellular and molecular medicine

2016 Volume 20, Issue 1, Page(s) 104–115

Abstract: The chemokine CXCL16 and its receptor CXCR6 have been linked to the pathogenesis of acute and chronic cardiovascular disease. However, data on the clinical significance of CXCL16 in patients undergoing cardiac surgery with acute myocardial ischemia/ ... ...

Abstract	The chemokine CXCL16 and its receptor CXCR6 have been linked to the pathogenesis of acute and chronic cardiovascular disease. However, data on the clinical significance of CXCL16 in patients undergoing cardiac surgery with acute myocardial ischemia/reperfusion (I/R) are still lacking. Therefore, we determined CXCL16 in the serum of cardiac surgery patients and investigated its kinetics and association with the extent of organ dysfunction. 48 patients underwent conventional cardiac surgery with myocardial I/R and the use of cardiopulmonary bypass (CPB) were consecutively enrolled in the present study. We investigated the peri- and post-operative profile of CXCL16. Clinical relevant data were assessed and documented throughout the entire observation period. To identify the influence of myocardial I/R and CPB on CXCL16 release data were compared to those received from patients that underwent off-pump procedure. Pre-operative serum CXCL16 levels were comparable to those obtained from healthy volunteers (1174 ± 55.64 pg/ml versus 1225 ± 70.94). However, CXCL16 levels significantly increased during surgery (1174 ± 55.64 versus 1442 ± 75.42 pg/ml; P = 0.0057) and reached maximum levels 6 hrs after termination of surgery (1174 ± 55.64 versus 1648 ± 74.71 pg/ml; P < 0.001). We revealed a positive correlation between the intraoperative serum levels of CXCL16 and the extent of organ dysfunction (r(2) = 0.356; P = 0.031). Patients with high CXCL16 release showed an increased extent of organ dysfunction compared to patients with low CXCL16 release. Our study shows that CXCL16 is released into the circulation as a result of cardiac surgery and that high post-operative CXCL16 levels are associated with an increased severity of post-operative organ dysfunctions.
MeSH term(s)	Aged ; Cells, Cultured ; Chemokine CXCL16 ; Chemokines, CXC/blood ; Female ; Heart Diseases/blood ; Heart Diseases/immunology ; Heart Diseases/surgery ; Humans ; Leukocyte Count ; Male ; Perioperative Period ; Postoperative Complications/blood ; Receptors, Scavenger/blood ; Systemic Inflammatory Response Syndrome/blood ; Treatment Outcome
Chemical Substances	CXCL16 protein, human ; Chemokine CXCL16 ; Chemokines, CXC ; Receptors, Scavenger
Language	English
Publishing date	2016-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.12708
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Article ; Online: Estrogen serum concentration affects blood immune cell composition and polarization in human females under controlled ovarian stimulation.

Habib, Pardes / Dreymueller, Daniela / Rösing, Benjamin / Botung, Hannes / Slowik, Alexander / Zendedel, Adib / Habib, Shahin / Hoffmann, Stefanie / Beyer, Cordian

The Journal of steroid biochemistry and molecular biology

2018 Volume 178, Page(s) 340–347

Abstract: Estrogens modulate the immune system and possess anti-inflammatory properties. In line, immune cells express a variety of estrogen receptors (ER) including ER-alpha and -beta. In the present study, we examined the influence of 17beta-estradiol (E2) serum ...

Abstract	Estrogens modulate the immune system and possess anti-inflammatory properties. In line, immune cells express a variety of estrogen receptors (ER) including ER-alpha and -beta. In the present study, we examined the influence of 17beta-estradiol (E2) serum concentrations on blood leukocyte composition and their ex vivo polarization/activation status by FACS analysis in sub-fertile human females under controlled ovarian stimulation (COS). Using a set of cell-type and polarization-specific markers, we demonstrate that increased 17ß-estradiol (E2) serum concentrations yield an overall increase in leukocytes, neutrophils and monocytes but decreased lymphocytes. There was a clear ratio shift towards an increase in M2 monocytes with a protective quality and an increase in T-helper cells compared to a decrease in cytotoxic T-cells. These data support experimental findings and clinical trials, i.e. related to multiple sclerosis and other autoimmune-related diseases, that have shown a down-regulation of CD8(+) T cells and up-regulation of T-regulatory cells. Further studies have to pinpoint to which extent the immune system/-responsiveness of otherwise healthy female patients is affected by medium-term systemic E2 variations.
MeSH term(s)	CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Cells, Cultured ; Estrogens/blood ; Female ; Humans ; Infertility, Female/blood ; Infertility, Female/immunology ; Infertility, Female/pathology ; Leukocytes/immunology ; Leukocytes/metabolism ; Neutrophils/immunology ; Neutrophils/metabolism ; Ovulation Induction ; Receptors, Estrogen/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
Chemical Substances	Estrogens ; Receptors, Estrogen
Language	English
Publishing date	2018-02-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2018.02.005
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Article ; Online: Sex steroid hormone-mediated functional regulation of microglia-like BV-2 cells during hypoxia.

Habib, Pardes / Dreymueller, Daniela / Ludwig, Andreas / Beyer, Cordian / Dang, Jon

The Journal of steroid biochemistry and molecular biology

2013 Volume 138, Page(s) 195–205

Abstract: 17β-estradiol (E2) and progesterone (P) are neuroprotective hormones in different neurological disorders and in particular under hypoxic conditions in the brain. Both hormones dampen brain-intrinsic immune responses and regulate local glial cell function. ...

Abstract	17β-estradiol (E2) and progesterone (P) are neuroprotective hormones in different neurological disorders and in particular under hypoxic conditions in the brain. Both hormones dampen brain-intrinsic immune responses and regulate local glial cell function. Besides astrocytes which are functionally regulated in a manifold and complex manner, especially microglial cells are in the focus of steroid-mediated neuroprotection. In previous studies using a transient brain artery occlusion model, we demonstrated that microglial characteristics are critically modified after the administration of either E2 or P. We here studied the influence of sex steroids on the murine BV-2 microglia cell line under hypoxic conditions. Hypoxia changed the cell morphology from an amoeboid-like phenotype with processes to a rounded shape of secreting cell type. BV-2 cells expressed both estrogen receptor-β and progesterone receptors under each condition. Oxygen deprivation increased the expression of inducible nitric oxide synthetase (iNOS) and up-regulated selected cytokines and chemokines. Both hormones selectively prevented the induction of pro-inflammatory iNOS, interleukin IL-1ß, and chemokine ligand CCL5, whereas anti-inflammatory IL-10 and protective TREM 2 were up-regulated by sex steroids. Sex hormones abrogated hypoxia-dependent reduction of BV-2 phagocytic activity. We demonstrate that BV-2 microglia cells respond to hypoxia by enhanced pro-inflammatory cytokine secretion and reduced phagocytic activity. This effect is prevented by sex steroids resulting in a switch of BV-2 cells from a pro-inflammatory to a more anti-inflammatory phenotype. Anti-inflammatory effects of gonadal steroids might directly be mediated through hormone-microglia interactions in addition to known effects via astroglial regulation.
MeSH term(s)	Animals ; Cell Hypoxia/drug effects ; Chemokine CCL5/metabolism ; Chemokines/metabolism ; Cytokines/metabolism ; Gonadal Steroid Hormones/pharmacology ; Interleukin-10/metabolism ; Interleukin-1beta/metabolism ; Mice ; Microglia/drug effects ; Microglia/metabolism ; Nitric Oxide Synthase Type II/metabolism
Chemical Substances	Chemokine CCL5 ; Chemokines ; Cytokines ; Gonadal Steroid Hormones ; Interleukin-1beta ; Interleukin-10 (130068-27-8) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2013-11
Publishing country	England
Document type	Journal Article
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2013.06.003
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Article ; Online: Embryonic stem cell-derived M2-like macrophages delay cutaneous wound healing.

Dreymueller, Daniela / Denecke, Bernd / Ludwig, Andreas / Jahnen-Dechent, Willi

Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society

2013 Volume 21, Issue 1, Page(s) 44–54

Abstract: In adults, repair of deeply injured skin wounds results in the formation of scar tissue, whereas in embryos wounds heal almost scar-free. Macrophages are important mediators of wound healing and secrete cytokines and tissue remodeling enzymes. In ... ...

Abstract	In adults, repair of deeply injured skin wounds results in the formation of scar tissue, whereas in embryos wounds heal almost scar-free. Macrophages are important mediators of wound healing and secrete cytokines and tissue remodeling enzymes. In contrast to host defense mediated by inflammatory M1 macrophages, wound healing and tissue repair involve regulatory M2/M2-like macrophages. Embryonic/fetal macrophages are M2-like, and this may promote scar-free wound healing. In the present study, we asked whether atopical application of ex vivo generated, embryonic stem cell-derived macrophages (ESDM) improve wound healing in mice. ESDM were tested side by side with bone marrow-derived macrophages (BMDM). Compared to BMDM, ESDM resembled a less inflammatory and more M2-like macrophage subtype as indicated by their reduced responsiveness to lipopolysaccharide, reduced expression of Toll-like receptors, and reduced bacterial phagocytosis. Despite this anti-inflammatory phenotype in cell culture, ESDM prolonged the healing of deep skin wounds even more than BMDM. Healed wounds had more scar formation compared to wounds receiving BMDM or cell-free treatment. Our data indicate that atopical application of ex vivo generated macrophages is not a suitable cell therapy of dermal wounds.
MeSH term(s)	Animals ; Cells, Cultured ; Cicatrix/pathology ; Cicatrix/therapy ; Disease Models, Animal ; Embryonic Stem Cells/transplantation ; Flow Cytometry ; Humans ; Inflammation/pathology ; Inflammation/therapy ; Macrophages/metabolism ; Mice ; Mice, Inbred C57BL ; Regeneration ; Skin/pathology ; Wound Healing ; Wounds and Injuries/pathology ; Wounds and Injuries/therapy
Language	English
Publishing date	2013-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1174873-4
ISSN	1524-475X ; 1067-1927
ISSN (online)	1524-475X
ISSN	1067-1927
DOI	10.1111/j.1524-475X.2012.00858.x
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