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Article: Age-dependent increase of oxidative stress regulates microRNA-29 family preserving cardiac health

Baumgart, Mario / Atlante, Sandra / Milano, Giuseppina / Scopece, Alessandro / Kuenne, Carsten / Braun, Thomas / Pompilio, Giulio / Martelli, Fabio / Zeiher, Andreas / Cellerino, Alessandro / Gaetano, Carlo / Spallotta, Francesco

Scientific reports, 7:16839

2017

Abstract: The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging ...

Institution	Leibniz-Institut für Alternsforschung
Abstract	The short-lived turquoise killifish Nothobranchius furzeri (Nfu) is a valid model for aging studies. Here, we investigated its age-associated cardiac function. We observed oxidative stress accumulation and an engagement of microRNAs (miRNAs) in the aging heart. MiRNA-sequencing of 5 week (young), 12–21 week (adult) and 28–40 week (old) Nfu hearts revealed 23 up-regulated and 18 down-regulated miRNAs with age. MiR-29 family turned out as one of the most up-regulated miRNAs during aging. MiR-29 family increase induces a decrease of known targets like collagens and DNA methyl transferases (DNMTs) paralleled by 5´methyl-cytosine (5mC) level decrease. To further investigate miR-29 family role in the fish heart we generated a transgenic zebrafish model where miR-29 was knocked-down. In this model we found significant morphological and functional cardiac alterations and an impairment of oxygen dependent pathways by transcriptome analysis leading to hypoxic marker up-regulation. To get insights the possible hypoxic regulation of miR-29 family, we exposed human cardiac fibroblasts to 1% O2 levels. In hypoxic condition we found miR-29 down-modulation responsible for the accumulation of collagens and 5mC. Overall, our data suggest that miR-29 family up-regulation might represent an endogenous mechanism aimed at ameliorating the age-dependent cardiac damage leading to hypertrophy and fibrosis.
Keywords	Cardiovascular biology ; Cell biology
Language	English
Document type	Article
Database	Repository for Life Sciences

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Article ; Online: Epigenetic Signaling and RNA Regulation in Cardiovascular Diseases.

Mongelli, Alessia / Atlante, Sandra / Bachetti, Tiziana / Martelli, Fabio / Farsetti, Antonella / Gaetano, Carlo

International journal of molecular sciences

2020 Volume 21, Issue 2

Abstract: RNA epigenetics is perhaps the most recent field of interest for translational epigeneticists. RNA modifications create such an extensive network of epigenetically driven combinations whose role in physiology and pathophysiology is still far from being ... ...

Abstract	RNA epigenetics is perhaps the most recent field of interest for translational epigeneticists. RNA modifications create such an extensive network of epigenetically driven combinations whose role in physiology and pathophysiology is still far from being elucidated. Not surprisingly, some of the players determining changes in RNA structure are in common with those involved in DNA and chromatin structure regulation, while other molecules seem very specific to RNA. It is envisaged, then, that new small molecules, acting selectively on RNA epigenetic changes, will be reported soon, opening new therapeutic interventions based on the correction of the RNA epigenetic landscape. In this review, we shall summarize some aspects of RNA epigenetics limited to those in which the potential clinical translatability to cardiovascular disease is emerging.
MeSH term(s)	Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Epigenesis, Genetic ; Humans ; Nucleic Acid Conformation ; RNA/genetics ; RNA/metabolism ; Signal Transduction/genetics
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2020-01-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21020509
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Article ; Online: The epigenetic implication in coronavirus infection and therapy.

Atlante, Sandra / Mongelli, Alessia / Barbi, Veronica / Martelli, Fabio / Farsetti, Antonella / Gaetano, Carlo

Clinical epigenetics

2020 Volume 12, Issue 1, Page(s) 156

Abstract: Epigenetics is a relatively new field of science that studies the genetic and non-genetic aspects related to heritable phenotypic changes, frequently caused by environmental and metabolic factors. In the host, the epigenetic machinery can regulate gene ... ...

Abstract	Epigenetics is a relatively new field of science that studies the genetic and non-genetic aspects related to heritable phenotypic changes, frequently caused by environmental and metabolic factors. In the host, the epigenetic machinery can regulate gene expression through a series of reversible epigenetic modifications, such as histone methylation and acetylation, DNA/RNA methylation, chromatin remodeling, and non-coding RNAs. The coronavirus disease 19 (COVID-19) is a highly transmittable and pathogenic viral infection. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which emerged in Wuhan, China, and spread worldwide, causes it. COVID-19 severity and consequences largely depend on patient age and health status. In this review, we will summarize and comparatively analyze how viruses regulate the host epigenome. Mainly, we will be focusing on highly pathogenic respiratory RNA virus infections such as coronaviruses. In this context, epigenetic alterations might play an essential role in the onset of coronavirus disease complications. Although many therapeutic approaches are under study, more research is urgently needed to identify effective vaccine or safer chemotherapeutic drugs, including epigenetic drugs, to cope with this viral outbreak and to develop pre- and post-exposure prophylaxis against COVID-19.
MeSH term(s)	Antiviral Agents/pharmacology ; Betacoronavirus/physiology ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/genetics ; Coronavirus Infections/immunology ; Cytokines/genetics ; Cytokines/immunology ; Epigenesis, Genetic ; Gene Expression Regulation, Viral/drug effects ; Host-Pathogen Interactions ; Humans ; Inflammation/immunology ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/genetics ; Pneumonia, Viral/immunology ; RNA Processing, Post-Transcriptional ; SARS-CoV-2
Chemical Substances	Antiviral Agents ; Cytokines
Keywords	covid19
Language	English
Publishing date	2020-10-21
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-020-00946-x
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Article ; Online: Treating Senescence like Cancer: Novel Perspectives in Senotherapy of Chronic Diseases.

Mongelli, Alessia / Atlante, Sandra / Barbi, Veronica / Bachetti, Tiziana / Martelli, Fabio / Farsetti, Antonella / Gaetano, Carlo

International journal of molecular sciences

2020 Volume 21, Issue 21

Abstract: The WHO estimated around 41 million deaths worldwide each year for age-related non-communicable chronic diseases. Hence, developing strategies to control the accumulation of cell senescence in living organisms and the overall aging process is an urgently ...

Abstract	The WHO estimated around 41 million deaths worldwide each year for age-related non-communicable chronic diseases. Hence, developing strategies to control the accumulation of cell senescence in living organisms and the overall aging process is an urgently needed problem of social relevance. During aging, many biological processes are altered, which globally induce the dysfunction of the whole organism. Cell senescence is one of the causes of this modification. Nowadays, several drugs approved for anticancer therapy have been repurposed to treat senescence, and others are under scrutiny in vitro and in vivo to establish their senomorphic or senolytic properties. In some cases, this research led to a significant increase in cell survival or to a prolonged lifespan in animal models, at least. Senomorphics can act to interfere with a specific pathway in order to restore the appropriate cellular function, preserve viability, and to prolong the lifespan. On the other hand, senolytics induce apoptosis in senescent cells allowing the remaining non-senescent population to preserve or restore tissue function. A large number of research articles and reviews recently addressed this topic. Herein, we would like to focus attention on those chemical agents with senomorphic or senolytic properties that perspectively, according to literature, suggest a potential application as senotherapeutics for chronic diseases.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Cellular Senescence ; Chronic Disease/drug therapy ; Chronic Disease/mortality ; Clinical Trials as Topic ; Global Health ; Humans ; Neoplasms/drug therapy ; Neoplasms/mortality ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2020-10-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21217984
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Article ; Online: Analysis of the Gadolinium retention in the Experimental Autoimmune Encephalomyelitis (EAE) murine model of Multiple Sclerosis.

Furlan, Chiara / Montarolo, Francesca / Di Gregorio, Enza / Parolisi, Roberta / Atlante, Sandra / Buffo, Annalisa / Bertolotto, Antonio / Aime, Silvio / Gianolio, Eliana

Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)

2021 Volume 68, Page(s) 126831

Abstract: Objectives: The aim of this study is to quantitatively investigate, at the preclinical level, the extent of Gd retention in the CNS, and peripheral organs, of immune-mediated murine models (Experimental Autoimmune Encephalomyelitis -EAE) of Multiple ... ...

Abstract	Objectives: The aim of this study is to quantitatively investigate, at the preclinical level, the extent of Gd retention in the CNS, and peripheral organs, of immune-mediated murine models (Experimental Autoimmune Encephalomyelitis -EAE) of Multiple Sclerosis, compared to control animals, upon the injection of gadodiamide. The influence of the Gadolinium Based Contrast Agent administration timing during the course of EAE development is also monitored. Methods: EAE mice were injected with three doses (1.2 mmol/kg each) of gadodiamide at three different time points during the EAE development and sacrificed after 21 or 39 days. Organs were collected and the amount of Gd was quantified through Inductively Coupled Plasma-Mass Spectrometry. Transmission electron microscopy (TEM) and MRI techniques were applied to add spatial and qualitative information to the obtained results. Results: In the spinal cord of EAE group, 21 days after gadodiamide administration, a significantly higher accumulation of Gd occurred. Conversely, in the encephalon, a lower amount of Gd retention was reached, even if differences emerged between EAE and controls mice. After 39 days, the amounts of retained Gd markedly decreased. TEM validated the presence of Gd in CNS. MRI of the encephalon at 7.1T did not highlight any hyper intense region. Conclusion: In the spinal cord of EAE mice, which is the mostly damaged region in this specific animal model, a preferential but transient accumulation of Gd is observed. In the encephalon, the Gd retention could be mostly related to inflammation occurring upon immunization rather than to demyelination.
MeSH term(s)	Animals ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental ; Gadolinium ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/diagnostic imaging ; Organometallic Compounds
Chemical Substances	Organometallic Compounds ; Gadolinium (AU0V1LM3JT)
Language	English
Publishing date	2021-08-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1236267-0
ISSN	1878-3252 ; 1611-602X ; 0946-672X
ISSN (online)	1878-3252 ; 1611-602X
ISSN	0946-672X
DOI	10.1016/j.jtemb.2021.126831
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Article ; Online: Gadolinium Retention in Erythrocytes and Leukocytes From Human and Murine Blood Upon Treatment With Gadolinium-Based Contrast Agents for Magnetic Resonance Imaging.

Di Gregorio, Enza / Furlan, Chiara / Atlante, Sandra / Stefania, Rachele / Gianolio, Eliana / Aime, Silvio

Investigative radiology

2019 Volume 55, Issue 1, Page(s) 30–37

Abstract: Objectives: Being administered intravenously, the tissue that gadolinium-based contrast agents (GBCAs) for magnetic resonance imaging mostly encounter is blood. Herein, it has been investigated how much Gd is internalized by cellular blood components ... ...

Abstract	Objectives: Being administered intravenously, the tissue that gadolinium-based contrast agents (GBCAs) for magnetic resonance imaging mostly encounter is blood. Herein, it has been investigated how much Gd is internalized by cellular blood components upon the in vitro incubation of GBCAs in human blood or upon intravenous administration of GBCAs to healthy mice. We report results that show how the superb sensitivity of inductively coupled plasma-mass spectrometry (ICP-MS) allows the detection of very tiny amounts of GBCAs entering red blood cells (RBCs) and white blood cells (WBCs). This finding may introduce new insights in the complex matter relative to excretion and retention pathway of administered GBCAs. Materials and methods: The study was tackled by 2 independent approaches. First, human blood was incubated in vitro with 5 mM of GBCAs (gadoteridol, gadobenate dimeglumine, gadodiamide, and gadopentetate dimeglumine) for variable times (30 minutes, 1 hour, 2 hours, and 3 hours) at 37°C. Then, blood cell components were isolated by using the Ficoll Histopaque method, washed 3 times, mineralized, and analyzed by ICP-MS for total Gd quantification. Furthermore, blood components derived from human blood incubated with gadodiamide or gadoteridol underwent UPLC-MS (ultra performance liquid chromatography-mass spectrometry) analysis for determination of the amount of intact Gd-DTPA-BMA and Gd-HPDO3A. Second, the distribution of Gd in the blood components of healthy CD-1 mice was administered intravenously with a single dose (1.2 mmol/kg) of gadodiamide or gadoteridol. Blood samples were separated and processed at different time points (24 hours, 48 hours, 96 hours, and 10 days after GBCA administration). As for human blood, ICP-MS quantification of total Gd and UPLC-MS determination of the amount of intact GBCAs were carried out. Results: The amount of Gd taken up by RBCs and WBCs was well detectable by ICP-MS. The GBCAs seem to be able to cross the membrane by diffusion (RBCs) or, possibly, by macropinocytosis (WBCs). Ex vivo studies allowed it to be established that the structure of the different GBCAs were not relevant to determine the amount of Gd internalized in the cells. Although the amount of Gd steadily decreases over time in gadoteridol-labeled cells, in the case of gadodiamide, the amount of Gd in the cells does not decrease (even 10 days after the administration of the GBCA). Moreover, while gadoteridol maintains its structural integrity upon cellular uptake, in the case of gadodiamide, the amount of intact complex markedly decreases over time. Conclusions: The detection of significant amounts of Gd in RBCs and WBCs indicates that GBCAs can cross blood cell membranes. This finding may play a role in our understanding of the processes that are at the basis of Gd retention in the tissues of patients who have received the administration of GBCAs.
MeSH term(s)	Animals ; Contrast Media/administration & dosage ; Contrast Media/pharmacokinetics ; Erythrocytes/metabolism ; Gadolinium/administration & dosage ; Gadolinium/pharmacokinetics ; Gadolinium DTPA/administration & dosage ; Gadolinium DTPA/pharmacokinetics ; Heterocyclic Compounds/administration & dosage ; Heterocyclic Compounds/pharmacokinetics ; Humans ; In Vitro Techniques ; Leukocytes/metabolism ; Magnetic Resonance Imaging ; Male ; Meglumine/administration & dosage ; Meglumine/analogs & derivatives ; Meglumine/pharmacokinetics ; Mice ; Models, Animal ; Organometallic Compounds/administration & dosage ; Organometallic Compounds/pharmacokinetics ; Spectrophotometry, Atomic/methods
Chemical Substances	Contrast Media ; Heterocyclic Compounds ; Organometallic Compounds ; gadoteridol (0199MV609F) ; gadobenic acid (15G12L5X8K) ; Meglumine (6HG8UB2MUY) ; gadodiamide (84F6U3J2R6) ; Gadolinium (AU0V1LM3JT) ; Gadolinium DTPA (K2I13DR72L)
Language	English
Publishing date	2019-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80345-5
ISSN	1536-0210 ; 0020-9996
ISSN (online)	1536-0210
ISSN	0020-9996
DOI	10.1097/RLI.0000000000000608
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Article ; Online: Epigenetic Signaling and RNA Regulation in Cardiovascular Diseases

Alessia Mongelli / Sandra Atlante / Tiziana Bachetti / Fabio Martelli / Antonella Farsetti / Carlo Gaetano

International Journal of Molecular Sciences, Vol 21, Iss 2, p

2020 Volume 509

Abstract	RNA epigenetics is perhaps the most recent field of interest for translational epigeneticists. RNA modifications create such an extensive network of epigenetically driven combinations whose role in physiology and pathophysiology is still far from being elucidated. Not surprisingly, some of the players determining changes in RNA structure are in common with those involved in DNA and chromatin structure regulation, while other molecules seem very specific to RNA. It is envisaged, then, that new small molecules, acting selectively on RNA epigenetic changes, will be reported soon, opening new therapeutic interventions based on the correction of the RNA epigenetic landscape. In this review, we shall summarize some aspects of RNA epigenetics limited to those in which the potential clinical translatability to cardiovascular disease is emerging.
Keywords	epigenetics ; nucleic acids ; rna ; dna ; cardiovascular disease ; chronic disease ; aging ; metabolism ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	612
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Treating Senescence Like Cancer

Alessia Mongelli / Sandra Atlante / Veronica Barbi / Tiziana Bachetti / Fabio Martelli / Antonella Farsetti / Carlo Gaetano

International Journal of Molecular Sciences, Vol 21, Iss 7984, p

Novel Perspectives in Senotherapy of Chronic Diseases

2020 Volume 7984

Abstract	The WHO estimated around 41 million deaths worldwide each year for age-related non-communicable chronic diseases. Hence, developing strategies to control the accumulation of cell senescence in living organisms and the overall aging process is an urgently needed problem of social relevance. During aging, many biological processes are altered, which globally induce the dysfunction of the whole organism. Cell senescence is one of the causes of this modification. Nowadays, several drugs approved for anticancer therapy have been repurposed to treat senescence, and others are under scrutiny in vitro and in vivo to establish their senomorphic or senolytic properties. In some cases, this research led to a significant increase in cell survival or to a prolonged lifespan in animal models, at least. Senomorphics can act to interfere with a specific pathway in order to restore the appropriate cellular function, preserve viability, and to prolong the lifespan. On the other hand, senolytics induce apoptosis in senescent cells allowing the remaining non–senescent population to preserve or restore tissue function. A large number of research articles and reviews recently addressed this topic. Herein, we would like to focus attention on those chemical agents with senomorphic or senolytic properties that perspectively, according to literature, suggest a potential application as senotherapeutics for chronic diseases.
Keywords	senolytics ; senomorphics ; chronic diseases ; aging ; senotherapeutics ; clinical trials ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	610
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: The epigenetic implication in coronavirus infection and therapy

Atlante, Sandra / Mongelli, Alessia / Barbi, Veronica / Martelli, Fabio / Farsetti, Antonella / Gaetano, Carlo

Clin Epigenetics

Abstract	Epigenetics is a relatively new field of science that studies the genetic and non-genetic aspects related to heritable phenotypic changes, frequently caused by environmental and metabolic factors. In the host, the epigenetic machinery can regulate gene expression through a series of reversible epigenetic modifications, such as histone methylation and acetylation, DNA/RNA methylation, chromatin remodeling, and non-coding RNAs. The coronavirus disease 19 (COVID-19) is a highly transmittable and pathogenic viral infection. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which emerged in Wuhan, China, and spread worldwide, causes it. COVID-19 severity and consequences largely depend on patient age and health status. In this review, we will summarize and comparatively analyze how viruses regulate the host epigenome. Mainly, we will be focusing on highly pathogenic respiratory RNA virus infections such as coronaviruses. In this context, epigenetic alterations might play an essential role in the onset of coronavirus disease complications. Although many therapeutic approaches are under study, more research is urgently needed to identify effective vaccine or safer chemotherapeutic drugs, including epigenetic drugs, to cope with this viral outbreak and to develop pre- and post-exposure prophylaxis against COVID-19.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #883596
Database	COVID19

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Article ; Online: Structural and biological characterization of new hybrid drugs joining an HDAC inhibitor to different NO-donors.

Atlante, Sandra / Chegaev, Konstantin / Cencioni, Chiara / Guglielmo, Stefano / Marini, Elisabetta / Borretto, Emily / Gaetano, Carlo / Fruttero, Roberta / Spallotta, Francesco / Lazzarato, Loretta

European journal of medicinal chemistry

2018 Volume 144, Page(s) 612–625

Abstract: HDAC inhibitors and NO donors have already revealed independently their broad therapeutic potential in pathologic contexts. Here we further investigated the power of their combination in a single hybrid molecule. Nitrooxy groups or substituted furoxan ... ...

Abstract	HDAC inhibitors and NO donors have already revealed independently their broad therapeutic potential in pathologic contexts. Here we further investigated the power of their combination in a single hybrid molecule. Nitrooxy groups or substituted furoxan derivatives were joined to the α-position of the pyridine ring of the selective class I HDAC inhibitor MS-275. Biochemical analysis showed that the association with the dinitrooxy compound 31 or the furoxan derivative 16 gives hybrid compounds the ability to preserve the single moiety activities. The two new hybrid molecules were then tested in a muscle differentiation assay. The hybrid compound bearing the moiety 31 promoted the formation of large myotubes characterized by highly multinucleated fibers, possibly due to a stimulation of myoblast fusion, as implicated by the strong induction of myomaker expression. Thanks to their unique biological features, these compounds may represent new therapeutic tools for cardiovascular, neuromuscular and inflammatory diseases.
MeSH term(s)	Animals ; Benzamides/chemical synthesis ; Benzamides/chemistry ; Benzamides/pharmacology ; Cell Differentiation/drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Histone Deacetylase Inhibitors/chemical synthesis ; Histone Deacetylase Inhibitors/chemistry ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Humans ; Mice ; Molecular Structure ; Muscle, Skeletal/cytology ; Muscle, Skeletal/drug effects ; Nitric Oxide/metabolism ; Pyridines/chemical synthesis ; Pyridines/chemistry ; Pyridines/pharmacology ; Structure-Activity Relationship
Chemical Substances	Benzamides ; Histone Deacetylase Inhibitors ; Pyridines ; entinostat (1ZNY4FKK9H) ; Nitric Oxide (31C4KY9ESH) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2018-01-20
Publishing country	France
Document type	Journal Article
ZDB-ID	188597-2
ISSN	1768-3254 ; 0009-4374 ; 0223-5234
ISSN (online)	1768-3254
ISSN	0009-4374 ; 0223-5234
DOI	10.1016/j.ejmech.2017.12.047
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