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Article ; Online: Exposure of the Gestating Mother to Sympathetic Stress Modifies the Cardiovascular Function of the Progeny in Male Rats.

Piquer, Beatriz / Olmos, Diandra / Flores, Andrea / Barra, Rafael / Bahamondes, Gabriela / Diaz-Araya, Guillermo / Lara, Hernan E

International journal of environmental research and public health

2023 Volume 20, Issue 5

Abstract: Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. ...

Abstract	Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function and sensitivity to in vivo adrenergic stimulation were studied in male progeny. Methods: Pregnant Sprague-Dawley rats were exposed to cold stress (4 °C/3 h/day); rats' male progeny were euthanized at 20 and 60 days old, and their hearts were used to determine the β-adrenergic receptor (βAR) (radioligand binding) and NE concentration. The in vivo arterial pressure response to isoproterenol (ISO, 1 mg/kg weight/day/10 days) was monitored in real time (microchip in the descending aorta). Results: Stressed male progeny presented no differences in ventricular weight, the cardiac NE was lower, and high corticosterone plasma levels were recorded at 20 and 60 days old. The relative abundance of β1 adrenergic receptors decreased by 36% and 45%, respectively ( Conclusion: These data suggest permanent changes to the heart's adrenergic response after rat progeny were stressed in the uterus.
MeSH term(s)	Rats ; Female ; Male ; Pregnancy ; Animals ; Humans ; Rats, Sprague-Dawley ; Mothers ; Placenta/metabolism ; Norepinephrine ; Receptors, Adrenergic, beta/metabolism ; Adrenergic Agents
Chemical Substances	Norepinephrine (X4W3ENH1CV) ; Receptors, Adrenergic, beta ; Adrenergic Agents
Language	English
Publishing date	2023-02-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph20054285
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Article ; Online: Senescent cardiac fibroblasts: A key role in cardiac fibrosis.

Osorio, José Miguel / Espinoza-Pérez, Claudio / Rimassa-Taré, Constanza / Machuca, Víctor / Bustos, Juan Ortega / Vallejos, Matías / Vargas, Héctor / Díaz-Araya, Guillermo

Biochimica et biophysica acta. Molecular basis of disease

2023 Volume 1869, Issue 4, Page(s) 166642

Abstract: Cardiac fibroblasts are a cell population that controls the homeostasis of the extracellular matrix and orchestrates a damage response to maintain cardiac architecture and performance. Due to these functions, fibroblasts play a central role in cardiac ... ...

Abstract	Cardiac fibroblasts are a cell population that controls the homeostasis of the extracellular matrix and orchestrates a damage response to maintain cardiac architecture and performance. Due to these functions, fibroblasts play a central role in cardiac fibrosis development, and there are large differences in matrix protein secretion profiles between fibroblasts from aged versus young animals. Senescence is a multifactorial and complex process that has been associated with inflammatory and fibrotic responses. After damage, transient cellular senescence is usually beneficial, as these cells promote tissue repair. However, the persistent presence of senescent cells within a tissue is linked with fibrosis development and organ dysfunction, leading to aging-related diseases such as cardiovascular pathologies. In the heart, early cardiac fibroblast senescence after myocardial infarction seems to be protective to avoid excessive fibrosis; however, in non-infarcted models of cardiac fibrosis, cardiac fibroblast senescence has been shown to be deleterious. Today, two new classes of drugs, termed senolytics and senostatics, which eliminate senescent cells or modify senescence-associated secretory phenotype, respectively, arise as novel therapeutical strategies to treat aging-related pathologies. However, further studies will be needed to evaluate the extent of the utility of senotherapeutic drugs in cardiac diseases, in which pathological context and temporality of the intervention must be considered.
MeSH term(s)	Animals ; Heart ; Cellular Senescence/physiology ; Aging/pathology ; Fibrosis ; Fibroblasts/metabolism
Language	English
Publishing date	2023-01-18
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2023.166642
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Article ; Online: Lipoxin A4 prevents high glucose-induced inflammatory response in cardiac fibroblast through FOXO1 inhibition.

González-Herrera, Fabiola / Anfossi, Renatto / Catalán, Mabel / Gutiérrez-Figueroa, Renata / Maya, Juan Diego / Díaz-Araya, Guillermo / Vivar, Raúl

Cellular signalling

2023 Volume 106, Page(s) 110657

Abstract: Cardiac cells respond to various pathophysiological stimuli, synthesizing inflammatory molecules that allow tissue repair and proper functioning of the heart; however, perpetuation of the inflammatory response can lead to cardiac fibrosis and heart ... ...

Abstract	Cardiac cells respond to various pathophysiological stimuli, synthesizing inflammatory molecules that allow tissue repair and proper functioning of the heart; however, perpetuation of the inflammatory response can lead to cardiac fibrosis and heart dysfunction. High concentration of glucose (HG) induces an inflammatory and fibrotic response in the heart. Cardiac fibroblasts (CFs) are resident cells of the heart that respond to deleterious stimuli, increasing the synthesis and secretion of both fibrotic and proinflammatory molecules. The molecular mechanisms that regulate inflammation in CFs are unknown, thus, it is important to find new targets that allow improving treatments for HG-induced cardiac dysfunction. NFκB is the master regulator of inflammation, while FoxO1 is a new participant in the inflammatory response, including inflammation induced by HG; however, its role in the inflammatory response of CFs is unknown. The inflammation resolution is essential for an effective tissue repair and recovery of the organ function. Lipoxin A4 (LXA4) is an anti-inflammatory agent with cytoprotective effects, while its cardioprotective effects have not been fully studied. Thus, in this study, we analyze the role of p65/NFκB, and FoxO1 in CFs inflammation induced by HG, evaluating the anti-inflammatory properties of LXA4. Our results demonstrated that HG induces the inflammatory response in CFs, using an in vitro and ex vivo model, while FoxO1 inhibition and silencing prevented HG effects. Additionally, LXA4 inhibited the activation of FoxO1 and p65/NFκB, and inflammation of CFs induced by HG. Therefore, our results suggest that FoxO1 and LXA4 could be novel drug targets for the treatment of HG-induced inflammatory and fibrotic disorders in the heart.
MeSH term(s)	Humans ; Lipoxins/pharmacology ; NF-kappa B ; Inflammation/drug therapy ; Fibrosis ; Glucose/toxicity ; Fibroblasts ; Forkhead Box Protein O1
Chemical Substances	lipoxin A4 ; Lipoxins ; NF-kappa B ; Glucose (IY9XDZ35W2) ; FOXO1 protein, human ; Forkhead Box Protein O1
Language	English
Publishing date	2023-03-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2023.110657
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Article ; Online: SGK1 is necessary to FoxO3a negative regulation, oxidative stress and cardiac fibroblast activation induced by TGF-β1.

González-Herrera, Fabiola / Catalán, Mabel / Anfossi, Renatto / Maya, Juan Diego / Pedrozo, Zully / Díaz-Araya, Guillermo / Vivar, Raúl

Cellular signalling

2023 Volume 109, Page(s) 110778

Abstract: Cardiac fibroblasts (CFs) activation is a common response to most pathological conditions affecting the heart, characterized by increased cellular secretory capacity and increased expression of fibrotic markers, such as collagen I and smooth muscle actin ...

Abstract	Cardiac fibroblasts (CFs) activation is a common response to most pathological conditions affecting the heart, characterized by increased cellular secretory capacity and increased expression of fibrotic markers, such as collagen I and smooth muscle actin type alpha (α-SMA). Fibrotic activation of CFs induces the increase in tissue protein content, with the consequent tissue stiffness, diastolic dysfunction, and heart failure. Therefore, the search for new mechanisms of CFs activation is important to find novel treatments for cardiac diseases characterized by fibrosis. In this regard, TGF-β1, a cytokine with proinflammatory and fibrotic properties, is crucial in the CFs activation and the development of fibrotic diseases, whereas its molecular targets are not completely known. Serum and glucocorticoid-regulated kinase (SGK1) is a protein involved in various pathophysiological phenomena, especially cardiac and renal diseases that curse with fibrosis. Additionally, SGK1 phosphorylates and regulates the activity and expression of several targets, highlighting FoxO3a for its role in the regulation of oxidative stress and CFs activation induced by TGF-β1. However, the regulation of SGK1 by TGF-β1 and its role in CFs activation have not been studied. In this work, we evaluate the role of SGK1 in CFs isolated from neonatal Sprague-Dawley rats. The participation of SGK1 in the fibrotic activation of CFs induced by TGF-β1 was analyzed, using an inhibitor or siRNA of SGK1. In addition, the role of SGK1 on the regulation of FoxO3a and oxidative stress induced by TGF-β1 was analyzed. Our results indicate that TGF-β1 increased both the activity and expression of SGK1 in CFs, requiring the activation of MAPKs, ERK1/2, p38 and JNK, while inhibition and silencing of SGK1 prevented TGF-β1-induced fibrotic activation of CFs. In addition, SGK1 inhibition prevented FoxO3a inactivation and expression reduction, catalase and SOD2 expression decrease, and the increase of oxidative stress induced by TGF-β1. Taken together, our results position SGK1 as an important regulator of CFs activation driven by TGF-β1, at least in part, through the regulation of FoxO3a and oxidative stress.
MeSH term(s)	Rats ; Animals ; Rats, Sprague-Dawley ; Myocardium/metabolism ; Transforming Growth Factor beta1/metabolism ; Oxidative Stress ; Fibroblasts/metabolism ; Fibrosis
Chemical Substances	Transforming Growth Factor beta1
Language	English
Publishing date	2023-06-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2023.110778
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Article: Silencing or not silencing

Díaz-Araya, Guillermo / Espitia-Corredor, Jenaro Antonio

Journal of thoracic disease

2018 Volume 10, Issue 10, Page(s) 5648–5651

Language	English
Publishing date	2018-06-25
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2573571-8
ISSN	2077-6624 ; 2072-1439
ISSN (online)	2077-6624
ISSN	2072-1439
DOI	10.21037/jtd.2018.09.13
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Article ; Online: Synthesis and Biological Evaluation of Novel Thiazolyl-Coumarin Derivatives as Potent Histone Deacetylase Inhibitors with Antifibrotic Activity.

Pardo-Jiménez, Viviana / Navarrete-Encina, Patricio / Díaz-Araya, Guillermo

Molecules (Basel, Switzerland)

2019 Volume 24, Issue 4

Abstract: New histone deacetylases (HDAC) inhibitors with low toxicity to non-cancerous cells, are a prevalent issue at present because these enzymes are actively involved in fibrotic diseases. We designed and synthesized a novel series of thiazolyl-coumarins, ... ...

Abstract	New histone deacetylases (HDAC) inhibitors with low toxicity to non-cancerous cells, are a prevalent issue at present because these enzymes are actively involved in fibrotic diseases. We designed and synthesized a novel series of thiazolyl-coumarins, substituted at position 6 (R = H, Br, OCH₃), linked to classic zinc binding groups, such as hydroxamic and carboxylic acid moieties and alternative zinc binding groups such as disulfide and catechol. Their in vitro inhibitory activities against HDACs were evaluated. Disulfide and hydroxamic acid derivatives were the most potent ones. Assays with neonatal rat cardiac fibroblasts demonstrated low cytotoxic effects for all compounds. Regarding the parameters associated to cardiac fibrosis development, the compounds showed antiproliferative effects, and triggered a strong decrease on the expression levels of both α-SMA and procollagen I. In conclusion, the new thiazolyl-coumarin derivatives inhibit HDAC activity and decrease profibrotic effects on cardiac fibroblasts.
MeSH term(s)	Animals ; Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Biomarkers ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Chemistry Techniques, Synthetic ; Coumarins/chemical synthesis ; Coumarins/chemistry ; Coumarins/pharmacology ; Fibrosis ; Gene Expression ; Histone Deacetylase Inhibitors/chemical synthesis ; Histone Deacetylase Inhibitors/chemistry ; Histone Deacetylase Inhibitors/pharmacology ; Inhibitory Concentration 50 ; Magnetic Resonance Spectroscopy ; Molecular Structure ; Rats
Chemical Substances	Antineoplastic Agents ; Biomarkers ; Coumarins ; Histone Deacetylase Inhibitors
Language	English
Publishing date	2019-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules24040739
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Article: Interferon-β decreases LPS-induced neutrophil recruitment to cardiac fibroblasts.

Anfossi, Renatto / Vivar, Raúl / Ayala, Pedro / González-Herrera, Fabiola / Espinoza-Pérez, Claudio / Osorio, José Miguel / Román-Torres, Mauricio / Bolívar, Samir / Díaz-Araya, Guillermo

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1122408

Abstract: Introduction: ...

Abstract	Introduction:
Language	English
Publishing date	2023-09-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1122408
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Article: Resolvin D1 and E1 promote resolution of inflammation in rat cardiac fibroblast in vitro

Salas-Hernández, Aimeé / Espinoza-Pérez, Claudio / Vivar, Raúl / Espitia-Corredor, Jenaro / Lillo, José / Parra-Flores, Pablo / Sánchez-Ferrer, Carlos F / Peiró, Concepción / Díaz-Araya, Guillermo

Molecular biology reports. 2021 Jan., v. 48, no. 1

2021

Abstract: Cardiac fibroblasts (CFs) have a key role in the inflammatory response after cardiac injury and are necessary for wound healing. Resolvins are potent agonists that control the duration and magnitude of inflammation. They decrease mediators of pro- ... ...

Abstract	Cardiac fibroblasts (CFs) have a key role in the inflammatory response after cardiac injury and are necessary for wound healing. Resolvins are potent agonists that control the duration and magnitude of inflammation. They decrease mediators of pro-inflammatory expression, reduce neutrophil migration to inflammation sites, promote the removal of microbes and apoptotic cells, and reduce exudate. However, whether resolvins can prevent pro-inflammatory-dependent effects in CFs is unknown. Thus, the present work was addressed to study whether resolvin D1 and E1 (RvD1 and RvE1) can prevent pro-inflammatory effects on CFs after lipopolysaccharide (LPS) challenge. For this, CFs were stimulated with LPS, in the presence or absence of RvD1 or RvE1, to analyze its effects on intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), monocyte adhesion and the cytokine levels of tumor necrosis factor alpha (TNF-α), interleukin-6(IL-6), interleukin-1beta (IL-1β), monocyte chemoattractant protein-1 (MCP-1) and interleukin-10 (IL-10). Our results showed that CFs are expressing ALX/FPR2 and ChemR23, RvD1 and RvE1 receptors, respectively. RvD1 and RvE1 prevent the increase of ICAM-1 and VCAM-1 protein levels and the adhesion of spleen mononuclear cells to CFs induced by LPS. Finally, RvD1, but not RvE1, prevents the LPS-induced increase of IL-6, MCP-1, TNF-α, and IL-10. In conclusion, our findings provide evidence that in CFs, RvD1 and RvE1 might actively participate in the prevention of inflammatory response triggered by LPS.
Keywords	adhesion ; apoptosis ; cell adhesion ; chemokine CCL2 ; fibroblasts ; inflammation ; intercellular adhesion molecule-1 ; interleukin-10 ; interleukin-1beta ; interleukin-6 ; lipopolysaccharides ; molecular biology ; monocytes ; neutrophils ; rats ; spleen ; tumor necrosis factor-alpha ; vascular cell adhesion molecules
Language	English
Dates of publication	2021-01
Size	p. 57-66.
Publishing place	Springer Netherlands
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-020-06133-8
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Resolvin E1 attenuates doxorubicin-induced cardiac fibroblast senescence: A key role for IL-1β.

Espitia-Corredor, Jenaro A / Shamoon, Licia / Olivares-Silva, Francisco / Rimassa-Taré, Constanza / Muñoz-Rodríguez, Claudia / Espinoza-Pérez, Claudio / Sánchez-Ferrer, Carlos F / Peiró, Concepción / Díaz-Araya, Guillermo

Biochimica et biophysica acta. Molecular basis of disease

2022 Volume 1868, Issue 11, Page(s) 166525

Abstract: Cardiac fibroblasts (CFs) undergo senescence in reaction to different stressors, leading to a poor prognosis of cardiac disease. Doxorubicin (Doxo) is an antineoplastic drug with strong cardiotoxic effects, which induces IL-1β secretion and thus, ... ...

Abstract	Cardiac fibroblasts (CFs) undergo senescence in reaction to different stressors, leading to a poor prognosis of cardiac disease. Doxorubicin (Doxo) is an antineoplastic drug with strong cardiotoxic effects, which induces IL-1β secretion and thus, triggers a potent pro-inflammatory response. Doxo induces CFs senescence; however, the mechanisms are not fully understood. Different pharmacological strategies have been used to eliminate senescent cells by inducing their apoptosis or modifying their secretome. However, Resolvin E1 (RvE1), a lipid derivative resolutive mediator with potent anti-inflammatory effects has not been used before to prevent CFs senescence. CFs were isolated from adult male C57BL/6J mice and subsequently stimulated with Doxo, in the presence or absence of RvE1. Senescence-associated β-galactosidase activity (SA-β-gal), γ-H2A.X, p53, p21, and senescence-associated secretory phenotype (SASP) were evaluated. The involvement of the NLRP3 inflammasome/interleukin-1 receptor (IL-1R) signaling pathway on CFs senescence was studied using an NLRP3 inhibitor (MCC950) and an endogenous IL-1R antagonist (IR1A). Doxo is able to trigger CFs senescence, as evidenced by an increase of γ-H2A.X, p53, p21, and SA-β-gal, and changes in the SASP profile. These Doxo effects were prevented by RvE1. Doxo triggers IL-1β secretion, which was dependent on NLRP3 activation. Doxo-induced CFs senescence was partially blocked by MCC950 and IR1A. In addition, IL-1β also triggered CFs senescence, as evidenced by the increase of γ-H2A.X, p53, p21, SA-β-gal activity, and SASP. All these effects were also prevented by RvE1 treatment. CONCLUSION: These data show the anti-senescent role of RvE1 in Doxo-induced CFs senescence, which could be mediated by reducing IL-1β secretion.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Cellular Senescence ; Doxorubicin/pharmacology ; Eicosapentaenoic Acid/analogs & derivatives ; Eicosapentaenoic Acid/pharmacology ; Fibroblasts/metabolism ; Furans ; Indenes ; Inflammasomes/metabolism ; Interleukin-1beta/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Receptors, Interleukin-1/metabolism ; Sulfonamides ; Tumor Suppressor Protein p53/metabolism ; beta-Galactosidase/metabolism ; beta-Galactosidase/pharmacology
Chemical Substances	Anti-Inflammatory Agents ; Furans ; IL1B protein, mouse ; Indenes ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Receptors, Interleukin-1 ; Sulfonamides ; Tumor Suppressor Protein p53 ; N-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamide (6RS86E2BWQ) ; Doxorubicin (80168379AG) ; Eicosapentaenoic Acid (AAN7QOV9EA) ; beta-Galactosidase (EC 3.2.1.23) ; 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid (GND3JH08JA)
Language	English
Publishing date	2022-08-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2022.166525
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Article ; Online: Resolvin E1 attenuates doxorubicin-induced endothelial senescence by modulating NLRP3 inflammasome activation.

Shamoon, Licia / Espitia-Corredor, Jenaro A / Dongil, Pilar / Menéndez-Ribes, Marta / Romero, Alejandra / Valencia, Inés / Díaz-Araya, Guillermo / Sánchez-Ferrer, Carlos F / Peiró, Concepción

Biochemical pharmacology

2022 Volume 201, Page(s) 115078

Abstract: Endothelial cell senescence contributes to chronic inflammation and endothelial dysfunction, while favoring cardiovascular disorders and frailty. Senescent cells acquire a pro-inflammatory secretory phenotype that further propagates inflammation and ... ...

Abstract	Endothelial cell senescence contributes to chronic inflammation and endothelial dysfunction, while favoring cardiovascular disorders and frailty. Senescent cells acquire a pro-inflammatory secretory phenotype that further propagates inflammation and senescence to neighboring cells. Cell senescence can be provoked by plethora of stressors, including inflammatory molecules and chemotherapeutic drugs. Doxorubicin (Doxo) is a powerful anthracycline anticancer drug whose clinical application is constrained by a dose-limiting cardiovascular toxicity. We here investigated whether cell senescence can contribute to the vascular damage elicited by Doxo. In human umbilical vein endothelial cells (HUVEC) cultures, Doxo (10-100 nM) increased the number of SA-β-gal positive cells and the levels of γH2AX, p21 and p53, used as markers of senescence. Moreover, we identified Doxo-induced senescence to be mediated by the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome, a key player of the immune innate system capable of releasing interleukin (IL)-1β. In fact, IL-1β itself mimicked the stimulatory action of Doxo on both NLRP3 activation and cellular senescence, while the pharmacological blockade of IL-1 receptors markedly attenuated the pro-senescence effects of Doxo. In search of additional pharmacological strategies to attenuate Doxo-induced endothelial senescence, we identified resolvin E1 (RvE1), an endogenous pro-resolving mediator, as capable of reducing cell senescence induced by both Doxo and IL-1β by interfering with the increased expression of pP65, NLRP3, and pro-IL-1β proteins and with the formation of active NLRP3 inflammasome complexes. Overall, RvE1 and the blockade of the NLRP3 inflammasome-IL-1β axis may offer a novel therapeutic approach against Doxo-induced cardiovascular toxicity and subsequent sequelae.
MeSH term(s)	Cellular Senescence/drug effects ; Doxorubicin/pharmacology ; Drug Interactions ; Eicosapentaenoic Acid/analogs & derivatives ; Eicosapentaenoic Acid/pharmacology ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/immunology ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Inflammasomes/drug effects ; Inflammasomes/immunology ; Inflammasomes/metabolism ; Inflammation/chemically induced ; Interleukin-1beta/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Chemical Substances	Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Doxorubicin (80168379AG) ; Eicosapentaenoic Acid (AAN7QOV9EA) ; 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid (GND3JH08JA)
Language	English
Publishing date	2022-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115078
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