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Article ; Online: Adenosine-to-inosine RNA editing controls cathepsin S expression in atherosclerosis by enabling HuR-mediated post-transcriptional regulation.

Stellos, Konstantinos / Gatsiou, Aikaterini / Stamatelopoulos, Kimon / Perisic Matic, Ljubica / John, David / Lunella, Federica Francesca / Jaé, Nicolas / Rossbach, Oliver / Amrhein, Carolin / Sigala, Frangiska / Boon, Reinier A / Fürtig, Boris / Manavski, Yosif / You, Xintian / Uchida, Shizuka / Keller, Till / Boeckel, Jes-Niels / Franco-Cereceda, Anders / Maegdefessel, Lars /

Chen, Wei / Schwalbe, Harald / Bindereif, Albrecht / Eriksson, Per / Hedin, Ulf / Zeiher, Andreas M / Dimmeler, Stefanie

Nature medicine

2016 Volume 22, Issue 10, Page(s) 1140–1150

Abstract: ... However, the role of A-to-I RNA editing in vascular disease is unknown. Here we show that cathepsin S mRNA (CTSS ...

Abstract	Adenosine-to-inosine (A-to-I) RNA editing, which is catalyzed by a family of adenosine deaminase acting on RNA (ADAR) enzymes, is important in the epitranscriptomic regulation of RNA metabolism. However, the role of A-to-I RNA editing in vascular disease is unknown. Here we show that cathepsin S mRNA (CTSS), which encodes a cysteine protease associated with angiogenesis and atherosclerosis, is highly edited in human endothelial cells. The 3' untranslated region (3' UTR) of the CTSS transcript contains two inverted repeats, the AluJo and AluSx
MeSH term(s)	3' Untranslated Regions ; Adenosine/metabolism ; Adenosine Deaminase/genetics ; Adult ; Aged ; Aged, 80 and over ; Aortic Aneurysm/genetics ; Atherosclerosis/genetics ; Carotid Artery Diseases/genetics ; Cathepsins/genetics ; Coronary Artery Disease/genetics ; ELAV-Like Protein 1/genetics ; Female ; Fluorescent Antibody Technique ; Gene Expression Regulation ; Gene Knock-In Techniques ; Gene Knockdown Techniques ; High-Throughput Nucleotide Sequencing ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypoxia/genetics ; Immunoblotting ; Inosine/metabolism ; Interferon-gamma/pharmacology ; Male ; Middle Aged ; RNA Editing/drug effects ; RNA Editing/genetics ; RNA Processing, Post-Transcriptional/drug effects ; RNA Processing, Post-Transcriptional/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/genetics ; Real-Time Polymerase Chain Reaction ; Sequence Analysis, RNA ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	3' Untranslated Regions ; ELAV-Like Protein 1 ; ELAVL1 protein, human ; RNA, Messenger ; RNA-Binding Proteins ; Tumor Necrosis Factor-alpha ; Inosine (5A614L51CT) ; Interferon-gamma (82115-62-6) ; Cathepsins (EC 3.4.-) ; cathepsin S (EC 3.4.22.27) ; ADAR protein, human (EC 3.5.4.37) ; Adenosine Deaminase (EC 3.5.4.4) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2016-09-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.4172
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Zs.A 4212: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Herz und Blut: klonale Hämatopoese.

Dimmeler, Stefanie / Zeiher, Andreas

Herz

2024 Volume 49, Issue 2, Page(s) 105–110

Abstract: Cardiovascular diseases are among the leading causes of death worldwide, with well-known modifiable risk factors, such as smoking, overweight, lipid metabolism disorders, lack of physical activity and high blood pressure playing a significant role. ... ...

Title translation	Heart and blood: clonal hematopoiesis.
Abstract	Cardiovascular diseases are among the leading causes of death worldwide, with well-known modifiable risk factors, such as smoking, overweight, lipid metabolism disorders, lack of physical activity and high blood pressure playing a significant role. Recent studies have now identified "clonal hematopoiesis" as a novel blood-based risk factor. Clonal hematopoiesis arises from mutations in hematopoietic stem cells, which lead to the expansion of mutated blood cells. Mutated cell clones can be detected in over 40% of individuals over 50 years old, with more than 15% of those over 90 years old harboring large clones. Surprisingly, mutated cells predispose to the development of leukemia only to a minor extent, leading to the term clonal hematopoiesis of indeterminate potential (CHIP); however, it has been shown that CHIP is associated with an increased risk of cardiovascular diseases. Individuals with CHIP-associated gene mutations have an elevated risk of atherosclerotic vascular diseases, stroke and thrombosis. Patients with heart failure with reduced ejection fraction (HFrEF), whether of ischemic or non-ischemic origin and patients with heart failure with preserved ejection fraction (HFpEF) exhibit an increased number of mutated cells in the blood. The presence of CHIP mutations is linked to a poorer prognosis in patients with existing cardiovascular diseases. Future research should aim at a better understanding of the specific effects of different mutations, clone sizes and combinations to develop personalized therapeutic approaches. Various anti-inflammatory therapeutic drugs are available, which can be tested in controlled studies.
MeSH term(s)	Humans ; Middle Aged ; Aged, 80 and over ; Clonal Hematopoiesis/genetics ; Cardiovascular Diseases/genetics ; Heart Failure/complications ; Hematopoiesis/genetics ; Stroke Volume ; Mutation/genetics
Language	German
Publishing date	2024-02-29
Publishing country	Germany
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	8262-4
ISSN	1615-6692 ; 0340-9937 ; 0946-1299
ISSN (online)	1615-6692
ISSN	0340-9937 ; 0946-1299
DOI	10.1007/s00059-024-05237-2
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Zs.A 1270: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Why is endothelial resilience key to maintain cardiac health?

Tombor, Lukas S / Dimmeler, Stefanie

Basic research in cardiology

2022 Volume 117, Issue 1, Page(s) 35

Abstract: Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell ... ...

Abstract	Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell multi-omics, together with genetic lineage tracing, reveal a transcriptional and phenotypical adaptation to the injured microenvironment, which includes alterations in metabolic, mesenchymal, hematopoietic and pro-inflammatory signatures. The extent of transition in mesenchymal or hematopoietic cell lineages is still debated, but it is clear that several of the adaptive phenotypical changes are transient and endothelial cells revert back to a naïve cell state after resolution of injury responses. This resilience of endothelial cells to acute stress responses is important for preventing chronic dysfunction. Here, we summarize how endothelial cells adjust to injury and how this dynamic response contributes to repair and regeneration. We will highlight intrinsic and microenvironmental factors that contribute to endothelial cell resilience and may be targetable to maintain a functionally active, healthy microcirculation.
MeSH term(s)	Endothelial Cells/metabolism ; Humans ; Myocardial Infarction/metabolism ; Myocytes, Cardiac/metabolism
Language	English
Publishing date	2022-07-14
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-022-00941-8
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Article ; Online: A coalition to heal-the impact of the cardiac microenvironment.

Tzahor, Eldad / Dimmeler, Stefanie

Science (New York, N.Y.)

2022 Volume 377, Issue 6610, Page(s) eabm4443

Abstract: Heart regenerative medicine has been gradually evolving from a view of the heart as a nonregenerative organ with terminally differentiated cardiac muscle cells. Understanding the biology of the heart during homeostasis and in response to injuries has led ...

Abstract	Heart regenerative medicine has been gradually evolving from a view of the heart as a nonregenerative organ with terminally differentiated cardiac muscle cells. Understanding the biology of the heart during homeostasis and in response to injuries has led to the realization that cellular communication between all cardiac cell types holds great promise for treatments. Indeed, recent studies highlight new disease-reversion concepts in addition to cardiomyocyte renewal, such as matrix- and vascular-targeted therapies, and immunotherapy with a focus on inflammation and fibrosis. In this review, we will discuss the cross-talk within the cardiac microenvironment and how specific therapies aim to target the hostile cardiac milieu under pathological conditions.
MeSH term(s)	Animals ; Cell Communication ; Cell Differentiation ; Heart Diseases/therapy ; Humans ; Mice ; Myocytes, Cardiac/physiology ; Regeneration/physiology ; Regenerative Medicine/trends
Language	English
Publishing date	2022-09-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	128410-1
ISSN	1095-9203 ; 0036-8075
ISSN (online)	1095-9203
ISSN	0036-8075
DOI	10.1126/science.abm4443
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Article: TNFalpha and oxLDL reduce protein S-nitrosylation in endothelial cells.

Hoffmann, J / Haendeler, J / Zeiher, A M / Dimmeler, S

The Journal of biological chemistry

2001 Volume 276, Issue 44, Page(s) 41383–41387

Abstract: ... of the endothelium. The intracellular reaction of NO with reactive cysteine groups leads to the formation of S ... nitrosothiols. To investigate the regulation of S-nitrosothiols in endothelial cells, we first analyzed ... the composition of the S-nitrosylated molecules in endothelial cells. Gel filtration revealed that more than 95 ...

Abstract	Nitric oxide (NO) plays an important role in the regulation of the functional integrity of the endothelium. The intracellular reaction of NO with reactive cysteine groups leads to the formation of S-nitrosothiols. To investigate the regulation of S-nitrosothiols in endothelial cells, we first analyzed the composition of the S-nitrosylated molecules in endothelial cells. Gel filtration revealed that more than 95% of the detected S-nitrosothiols had a molecular mass of more than 5000 Da. Moreover, inhibition of de novo synthesis of glutathione using N-butyl-sulfoximine did not diminish the overall cellular S-NO content suggesting that S-nitrosylated glutathione quantitatively plays only a minor role in endothelial cells. Having demonstrated that most of the S-nitrosothiols are proteins, we determined the regulation of the S-nitrosylation by pro-inflammatory and pro-atherogenic factors, such as TNFalpha and mildly oxidized low density lipoprotein (oxLDL). TNFalpha and oxLDL induced denitrosylation of various proteins as assessed by Saville-Griess assay, by immunostaining with an anti-S-nitrosocysteine antibody, and by a Western blot approach. Furthermore, the caspase-3 p17 subunit, which has previously been shown to be S-nitrosylated and thereby inhibited, was denitrosylated by TNFalpha treatment suggesting that S-nitrosylation and denitrosylation are important regulatory mechanisms in endothelial cells contributing to the integrity of the endothelial cell monolayer.
MeSH term(s)	Blotting, Western ; Chromatography, Gel ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Humans ; Lipoproteins, LDL/metabolism ; Molecular Weight ; S-Nitrosothiols/chemistry ; S-Nitrosothiols/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Lipoproteins, LDL ; S-Nitrosothiols ; Tumor Necrosis Factor-alpha ; oxidized low density lipoprotein
Language	English
Publishing date	2001-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M107566200
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Article ; Online: Noncoding RNAs in the Vasculature: Basic Mechanisms and Therapeutic Perspectives.

Maegdefessel, Lars / Boon, Reinier A / Dimmeler, Stefanie

Arteriosclerosis, thrombosis, and vascular biology

2023 Volume 44, Issue 1, Page(s) 3–6

MeSH term(s)	RNA, Untranslated/genetics ; MicroRNAs/genetics ; RNA, Long Noncoding ; Epigenesis, Genetic
Chemical Substances	RNA, Untranslated ; MicroRNAs ; RNA, Long Noncoding
Language	English
Publishing date	2023-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.123.319564
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Article ; Online: SARS-CoV-2 induced vascular endothelial dysfunction: direct or indirect effects?

Lui, Kathy O / Ma, Zhangjing / Dimmeler, Stefanie

Cardiovascular research

2023 Volume 120, Issue 1, Page(s) 34–43

Abstract: Clinical evidence reveals that manifestations of endothelial dysfunction are widely observed in COVID-19 and long-COVID patients. However, whether these detrimental effects are caused by direct infection of the endothelium or are indirectly mediated by ... ...

Abstract	Clinical evidence reveals that manifestations of endothelial dysfunction are widely observed in COVID-19 and long-COVID patients. However, whether these detrimental effects are caused by direct infection of the endothelium or are indirectly mediated by systemic inflammation has been a matter of debate. It has been well acknowledged that endothelial cells (ECs) of the cardiovascular system ubiquitously express the SARS-CoV-2 entry receptor angiotensin-converting enzyme 2 (ACE2), yet accumulating evidence suggests that it is more predominantly expressed by pericytes and vascular smooth muscle cells of the mammalian blood vessel. Besides, replicative infection of ECs by SARS-CoV-2 has yet to be demonstrated both in vitro and in vivo. In this study, we review latest research on endothelial ACE2 expression in different vascular beds, and the heterogeneity in various EC subsets with differential ACE2 expression in response to SARS-CoV-2. We also discuss ACE2-independent alternative mechanisms underlying endothelial activation in COVID-19, and the clinical manifestations of SARS-CoV-2-induced endothelial dysfunction. Altogether, understanding ACE2-dependent and ACE2-independent mechanisms driving SARS-CoV-2-induced vascular dysfunction would shed light on strategies of more effective therapies targeting cardiovascular complications associated with COVID-19.
MeSH term(s)	Animals ; Humans ; SARS-CoV-2/metabolism ; COVID-19 ; Angiotensin-Converting Enzyme 2/metabolism ; Endothelial Cells/metabolism ; Post-Acute COVID-19 Syndrome ; Peptidyl-Dipeptidase A/metabolism ; Vascular Diseases ; Mammals/metabolism
Chemical Substances	Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Peptidyl-Dipeptidase A (EC 3.4.15.1)
Language	English
Publishing date	2023-12-29
Publishing country	England
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvad191
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Article ; Online: Antioxidant effects of statins via S-nitrosylation and activation of thioredoxin in endothelial cells: a novel vasculoprotective function of statins.

Haendeler, Judith / Hoffmann, Jörg / Zeiher, Andreas M / Dimmeler, Stefanie

Circulation

2004 Volume 110, Issue 7, Page(s) 856–861

Abstract: ... pleiotropic vasculoprotective effects via activation of the endothelial NO synthesis. NO induces S ... nitrosylation of target proteins. S-Nitrosylation of the antioxidant enzyme thioredoxin was recently shown ... whether statins may exert an antioxidant activity in endothelial cells via S-nitrosylation of thioredoxin ...

Abstract	Background: HMG-CoA reductase inhibitors (statins) are lipid-lowering drugs that also exert pleiotropic vasculoprotective effects via activation of the endothelial NO synthesis. NO induces S-nitrosylation of target proteins. S-Nitrosylation of the antioxidant enzyme thioredoxin was recently shown to enhance its activity, thereby reducing intracellular reactive oxygen species. Therefore, we investigated whether statins may exert an antioxidant activity in endothelial cells via S-nitrosylation of thioredoxin. Methods and results: Statins dose- and time-dependently increased the overall level of S-nitrosylated proteins in endothelial cells (atorvastatin 0.1 micromol/L, 206+/-30% increase; simvastatin 1 micromol/L, 214+/-19% increase; mevastatin 1 micromol/L, 191+/-10% increase). The increased S-nitrosylation was blocked by an NO-synthase inhibitor and mevalonate. Moreover, S-nitrosylation of thioredoxin was also significantly augmented after atorvastatin treatment. The atorvastatin-mediated increase in S-nitrosylation was associated with an enhanced enzymatic activity of thioredoxin (atorvastatin, 157+/-9% increase). This resulted in a significant reduction of intracellular reactive oxygen species within the endothelial cells. In contrast, in endothelial cells overexpressing a thioredoxin construct in which the S-nitrosylation acceptor amino acid cysteine 69 was replaced by serine [TRX(C69S)], atorvastatin did not activate the redox-regulatory activity of thioredoxin. Moreover, overexpression of the non-nitrosylatable thioredoxin TRX(C69S) abolished atorvastatin-mediated reduction of reactive oxygen species. Conclusions: Here, we demonstrate a novel antioxidant mechanism by which statins reduce reactive oxygen species in endothelial cells. Statin-mediated S-nitrosylation of thioredoxin enhanced the enzymatic activity of thioredoxin, resulting in a significant reduction in intracellular reactive oxygen species.
MeSH term(s)	Amino Acid Substitution ; Antioxidants/pharmacology ; Atorvastatin Calcium ; Cells, Cultured/drug effects ; Cells, Cultured/metabolism ; Cysteine/analogs & derivatives ; Cysteine/metabolism ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Heptanoic Acids/pharmacology ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Lovastatin/analogs & derivatives ; Lovastatin/pharmacology ; Mutagenesis, Site-Directed ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Oxidative Stress/drug effects ; Protein Processing, Post-Translational/drug effects ; Pyrroles/pharmacology ; Reactive Oxygen Species/metabolism ; Recombinant Fusion Proteins/drug effects ; Recombinant Fusion Proteins/metabolism ; S-Nitrosothiols/metabolism ; Simvastatin/pharmacology ; Thioredoxins/chemistry ; Thioredoxins/drug effects ; Thioredoxins/genetics ; Thioredoxins/metabolism ; Transfection ; Umbilical Veins
Chemical Substances	Antioxidants ; Heptanoic Acids ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Pyrroles ; Reactive Oxygen Species ; Recombinant Fusion Proteins ; S-Nitrosothiols ; mevastatin (1UQM1K0W9X) ; Nitric Oxide (31C4KY9ESH) ; Atorvastatin Calcium (48A5M73Z4Q) ; Thioredoxins (52500-60-4) ; S-nitrosocysteine (926P2322P4) ; Lovastatin (9LHU78OQFD) ; Simvastatin (AGG2FN16EV) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2004-08-17
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/01.CIR.0000138743.09012.93
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Article: Shear stress increases the amount of S-nitrosylated molecules in endothelial cells: important role for signal transduction.

Hoffmann, Jörg / Dimmeler, Stefanie / Haendeler, Judith

FEBS letters

2003 Volume 551, Issue 1-3, Page(s) 153–158

Abstract: ... in endothelial cells. NO can react with free SH-groups of different proteins leading to S-nitrosylation. Since S ... of endogenously synthesized NO. Exposure to shear stress significantly increased the overall S-nitrosylation ... of proteins in endothelial cells. Interestingly, shear stress increased S-nitrosylation of specific ...

Abstract	Laminar flow (shear stress) is an important stimulus for nitric oxide (NO) synthesis in endothelial cells. NO can react with free SH-groups of different proteins leading to S-nitrosylation. Since S-nitrosylation of proteins is an important regulator of protein functions, we investigated the effect of endogenously synthesized NO. Exposure to shear stress significantly increased the overall S-nitrosylation of proteins in endothelial cells. Interestingly, shear stress increased S-nitrosylation of specific target proteins, i.e. the catalytic p17 subunit of caspase-3, the GTPase p21ras and the oxidoreductase thioredoxin. S-nitrosylation resulted in an inhibition of caspase-3 and in an augmented activity of p21ras and thioredoxin. These data suggest that long term exposure to shear stress exerts its different atheroprotective effects at least in part via increased S-nitrosylation of specific signaling proteins.
MeSH term(s)	Caspase 3 ; Caspases/chemistry ; Cells, Cultured ; Cysteine/analogs & derivatives ; Cysteine/analysis ; Endothelium, Vascular/chemistry ; Endothelium, Vascular/metabolism ; Humans ; Proto-Oncogene Proteins p21(ras)/chemistry ; Proto-Oncogene Proteins p21(ras)/metabolism ; S-Nitrosothiols/analysis ; Signal Transduction ; Stress, Mechanical ; Thioredoxins/chemistry ; Thioredoxins/metabolism
Chemical Substances	S-Nitrosothiols ; Thioredoxins (52500-60-4) ; S-nitrosocysteine (926P2322P4) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspases (EC 3.4.22.-) ; HRAS protein, human (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Cysteine (K848JZ4886)
Language	English
Publishing date	2003-08-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/s0014-5793(03)00917-7
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Article ; Online: The endothelial niche in heart failure: from development to regeneration.

Wagner, Julian U G / Dimmeler, Stefanie

European heart journal

2021 Volume 42, Issue 41, Page(s) 4277–4279

MeSH term(s)	Heart Failure ; Humans ; Regeneration
Language	English
Publishing date	2021-08-12
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	603098-1
ISSN	1522-9645 ; 0195-668X
ISSN (online)	1522-9645
ISSN	0195-668X
DOI	10.1093/eurheartj/ehab304
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