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Article ; Online: Telomere shortening during human septic shock: influence of sepsis mediators, role in organ failures, and septic myocardial dysfunction.

Razazi, Keyvan / Marcos, Elisabeth / Hüe, Sophie / Boyer, Laurent / Adnot, Serge / Mekontso Dessap, Armand

2021 Volume 25, Issue 1, Page(s) 401

MeSH term(s)	Cardiomyopathies ; Humans ; Multiple Organ Failure ; Sepsis ; Shock, Septic/genetics ; Shock, Septic/physiopathology ; Telomere Shortening
Language	English
Publishing date	2021-11-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2041406-7
ISSN	1466-609X ; 1364-8535
ISSN (online)	1466-609X
ISSN	1364-8535
DOI	10.1186/s13054-021-03818-9
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Zs.A 5517: Show issues

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Article ; Online: Loss of Pla2r1 decreases cellular senescence and age-related alterations caused by aging and Western diets.

Massemin, Amélie / Goehrig, Delphine / Flaman, Jean-Michel / Jaber, Sara / Griveau, Audrey / Djebali, Sophia / Marcos, Elisabeth / Payen, Léa / Marvel, Jacqueline / Parent, Romain / Adnot, Serge / Bertolino, Philippe / Rieusset, Jennifer / Tortereau, Antonin / Vindrieux, David / Bernard, David

Aging cell

2023 Volume 22, Issue 11, Page(s) e13971

Abstract: Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of ... ...

Abstract	Cellular senescence is induced by many stresses including telomere shortening, DNA damage, oxidative, or metabolic stresses. Senescent cells are stably cell cycle arrested and they secrete many factors including cytokines and chemokines. Accumulation of senescent cells promotes many age-related alterations and diseases. In this study, we investigated the role of the pro-senescent phospholipase A2 receptor 1 (PLA2R1) in regulating some age-related alterations in old mice and in mice subjected to a Western diet, whereas aged wild-type mice displayed a decreased ability to regulate their glycemia during glucose and insulin tolerance tests, aged Pla2r1 knockout (KO) mice efficiently regulated their glycemia and displayed fewer signs of aging. Loss of Pla2r1 was also found protective against the deleterious effects of a Western diet. Moreover, these Pla2r1 KO mice were partially protected from diet-induced senescent cell accumulation, steatosis, and fibrosis. Together these results support that Pla2r1 drives several age-related alterations, especially in the liver, arising during aging or through a Western diet.
MeSH term(s)	Animals ; Mice ; Aging/genetics ; Cellular Senescence/genetics ; Diet, Western ; Mice, Knockout ; Telomere Shortening
Chemical Substances	Pla2r1 protein, mouse
Language	English
Publishing date	2023-09-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13971
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Zs.A 6581: Show issues

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Article ; Online: Shortening telomere is associated with psychotic dimensions in the general population.

Schürhoff, Franck / Corfdir, Cécile / Pignon, Baptiste / Lajnef, Mohamed / Richard, Jean-Romain / Marcos, Elisabeth / Leboyer, Marion / Adnot, Serge / Jamain, Stéphane / Szöke, Andreï

Schizophrenia research

2022 Volume 243, Page(s) 470–471

MeSH term(s)	Humans ; Mental Disorders ; Telomere/genetics ; Telomere Shortening
Language	English
Publishing date	2022-03-02
Publishing country	Netherlands
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2022.02.030
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Zs.A 2351: 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)
Zs.MO 543: Show issues

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Article ; Online: Heart Rate Control during Experimental Sepsis in Mice: Comparison of Ivabradine and β-Blockers.

Bedet, Alexandre / Voiriot, Guillaume / Ternacle, Julien / Marcos, Elisabeth / Adnot, Serge / Derumeaux, Geneviève / Mekontso Dessap, Armand

Anesthesiology

2020 Volume 132, Issue 2, Page(s) 321–329

Abstract: Background: Tachycardia is a hallmark of sepsis. An elevated heart rate could impair ventricular filling and increase myocardial oxygen demand. β-Blockers and ivabradine (a selective inhibitor of If channels in the sinoatrial node) are both able to ... ...

Abstract	Background: Tachycardia is a hallmark of sepsis. An elevated heart rate could impair ventricular filling and increase myocardial oxygen demand. β-Blockers and ivabradine (a selective inhibitor of If channels in the sinoatrial node) are both able to control sinus tachycardia, with the latter drug being devoid of negative inotropic effect. This work aimed at assessing the hemodynamic effects of ivabradine as compared with a β-blocker (atenolol) during murine peritonitis. Methods: Ivabradine (3 μg/g), atenolol (3 μg/g), or placebo was administered intraperitoneally 2 h after induction of peritonitis (cecal ligation and puncture) in male C57BL6 mice. The authors used invasive (left ventricular catheterization) and noninvasive (transthoracic echocardiography) monitoring to assess hemodynamics 20 h after surgery, including heart rate, blood pressure, left ventricular systolic, and diastolic function (n = 10 mice/group). The authors also assessed overall mortality 30 and 60 h after surgery in a distinct subset of animals (n = 20 mice/group). Descriptive data are presented as median (25th to 75th percentile). Results: As compared with placebo (601 beats/min [547 to 612]), ivabradine (447 beats/min [430 to 496]) and atenolol (482 beats/min [412 to 505]) blunted sepsis-induced tachycardia assessed by transthoracic echocardiography in awake animals (P < 0.001 and P = 0.004, respectively). Unlike ivabradine, atenolol reduced cardiac output, systolic blood pressure, and left ventricular systolic function (as assessed by ejection fraction, maximal left ventricular pressure rise, and anterior wall strain rate) as compared with septic mice receiving placebo. There was no difference in survival 60 h after sepsis induction with ivabradine (6 of 20, 30%) or atenolol (7 of 20, 35%), as compared with placebo (5 of 20, 25%; P = 0.224). Conclusions: Heart rate control could be similarly achieved by ivabradine or atenolol, with preservation of blood pressure, cardiac output, and left ventricular systolic function with the former drug.
MeSH term(s)	Adrenergic beta-Antagonists/pharmacology ; Adrenergic beta-Antagonists/therapeutic use ; Animals ; Cardiovascular Agents/pharmacology ; Cardiovascular Agents/therapeutic use ; Heart Rate/drug effects ; Heart Rate/physiology ; Ivabradine/pharmacology ; Ivabradine/therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Random Allocation ; Sepsis/drug therapy ; Sepsis/physiopathology
Chemical Substances	Adrenergic beta-Antagonists ; Cardiovascular Agents ; Ivabradine (3H48L0LPZQ)
Language	English
Publishing date	2020-01-14
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	269-0
ISSN	1528-1175 ; 0003-3022
ISSN (online)	1528-1175
ISSN	0003-3022
DOI	10.1097/ALN.0000000000003045
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Uk I Zs.133: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 199: Show issues

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Article ; Online: Eliminating Senescent Cells Can Promote Pulmonary Hypertension Development and Progression.

Born, Emmanuelle / Lipskaia, Larissa / Breau, Marielle / Houssaini, Amal / Beaulieu, Delphine / Marcos, Elisabeth / Pierre, Remi / Do Cruzeiro, Marcio / Lefevre, Marine / Derumeaux, Genevieve / Bulavin, Dmitry V / Delcroix, Marion / Quarck, Rozenn / Reen, Virinder / Gil, Jesus / Bernard, David / Flaman, Jean-Michel / Adnot, Serge / Abid, Shariq

Circulation

2022 Volume 147, Issue 8, Page(s) 650–666

Abstract: Background: Senescent cells (SCs) are involved in proliferative disorders, but their role in pulmonary hypertension remains undefined. We investigated SCs in patients with pulmonary arterial hypertension and the role of SCs in animal pulmonary ... ...

Abstract	Background: Senescent cells (SCs) are involved in proliferative disorders, but their role in pulmonary hypertension remains undefined. We investigated SCs in patients with pulmonary arterial hypertension and the role of SCs in animal pulmonary hypertension models. Methods: We investigated senescence (p16, p21) and DNA damage (γ-H2AX, 53BP1) markers in patients with pulmonary arterial hypertension and murine models. We monitored p16 activation by luminescence imaging in p16-luciferase (p16 Results: Patients with pulmonary arterial hypertension compared with controls exhibited high lung p16, p21, and γ-H2AX protein levels, with abundant vascular cells costained for p16, γ-H2AX, and 53BP1. Hypoxia increased thoracic bioluminescence in p16 Conclusions: Elimination of senescent P-ECs by senolytic interventions may worsen pulmonary hemodynamics. These results invite consideration of the potential impact on pulmonary vessels of strategies aimed at controlling cell senescence in various contexts.
MeSH term(s)	Mice ; Rats ; Animals ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/metabolism ; Pulmonary Arterial Hypertension/metabolism ; Endothelial Cells/metabolism ; Monocrotaline/metabolism ; Senotherapeutics ; Pulmonary Artery ; Familial Primary Pulmonary Hypertension/metabolism ; Hypoxia/metabolism ; Cellular Senescence ; Forkhead Transcription Factors/metabolism
Chemical Substances	navitoclax (XKJ5VVK2WD) ; Monocrotaline (73077K8HYV) ; Senotherapeutics ; FOXO4 protein, rat ; Forkhead Transcription Factors
Language	English
Publishing date	2022-12-14
Publishing country	United States
Document type	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/CIRCULATIONAHA.122.058794
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Ui IV Zs.60: Show issues

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Article ; Online: No alteration of leukocyte telomere length in first episode psychosis.

Schürhoff, Franck / Corfdir, Cécile / Pignon, Baptiste / Lajnef, Mohamed / Richard, Jean-Romain / Marcos, Elisabeth / Pelissolo, Antoine / Leboyer, Marion / Adnot, Serge / Jamain, Stephane / Szöke, Andrei

Psychiatry research

2021 Volume 301, Page(s) 113941

Abstract: Both shorter telomeres and schizophrenia have been associated with a decrease in life expectancy. Furthermore, several studies found a shorter telomere length (TL) in schizophrenia. Understanding whether or not telomere shortening is directly related to ... ...

Abstract	Both shorter telomeres and schizophrenia have been associated with a decrease in life expectancy. Furthermore, several studies found a shorter telomere length (TL) in schizophrenia. Understanding whether or not telomere shortening is directly related to pathophysiology of schizophrenia or is a consequence of a cumulative exposure to chronic stress is of major importance. Comparing the TL of subjects at the very beginning of the disease (FEP) and control subjects could help to decide between these two hypotheses. The aim of the present study was to compare TL between FEP subjects (N=91) and controls (N=137). After accounting for multiple potential confounders, no significant association was observed between FEP and TL. Our result is consistent with the hypothesis that psycho-social stress / adversities and stressful situations in people with schizophrenia affect TL rather than that telomere erosion contributes to the development of this disorder.
MeSH term(s)	Humans ; Leukocytes ; Psychotic Disorders/genetics ; Schizophrenia/genetics ; Telomere/genetics ; Telomere Shortening
Language	English
Publishing date	2021-04-18
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	445361-x
ISSN	1872-7123 ; 1872-7506 ; 0925-4927 ; 0165-1781
ISSN (online)	1872-7123 ; 1872-7506
ISSN	0925-4927 ; 0165-1781
DOI	10.1016/j.psychres.2021.113941
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Article ; Online: Phospholipase A2 receptor 1 promotes lung cell senescence and emphysema in obstructive lung disease.

The European respiratory journal

2021 Volume 58, Issue 2

Abstract: Background: Cell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence ... ...

Abstract	Background: Cell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence acting Methods: We assessed cell senescence in lungs and cultured lung cells from patients with COPD and controls subjected to Results: We found that Conclusions: Our data support a major role for PLA2R1 activation in driving lung cell senescence and lung alterations in COPD. Targeting JAK1/2 may represent a promising therapeutic approach for COPD.
MeSH term(s)	Animals ; Cellular Senescence ; Emphysema ; Humans ; Lung ; Mice ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Emphysema ; Receptors, Phospholipase A2
Chemical Substances	PLA2R1 protein, human ; Receptors, Phospholipase A2
Language	English
Publishing date	2021-08-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.00752-2020
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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Article: Serotonin transporter and serotonin receptors.

Adnot, Serge / Houssaini, Amal / Abid, Shariq / Marcos, Elisabeth / Amsellem, Valérie

Handbook of experimental pharmacology

2013 Volume 218, Page(s) 365–380

Abstract: The nature of the primary defect responsible for triggering and maintaining pulmonary artery smooth muscle (PA-SMC) proliferation in pulmonary artery hypertension (PAH) is poorly understood but may be either an inherent characteristic of PA-SMCs or a ... ...

Abstract	The nature of the primary defect responsible for triggering and maintaining pulmonary artery smooth muscle (PA-SMC) proliferation in pulmonary artery hypertension (PAH) is poorly understood but may be either an inherent characteristic of PA-SMCs or a secondary response to an external abnormality, such as upregulation of growth factors. The serotonin hypothesis of PAH originated in the 1960s after an outbreak of the disease was reported among patients taking the anorexigenic drugs aminorex. The anorexiant dexfenfluramine which inhibits 5-HT neuronal uptake, causes 5-HT platelet depletion, and increases plasma levels of 5-HT, was then shown to increase the relative risk of developing PAH in the adults. More recently, the incidence of persistent pulmonary hypertension of the newborn was shown to be increased by the use of selective 5-HT reuptake inhibitors taken in late pregnancy. Serotonin is a vasoconstrictor and a potent mitogen for pulmonary smooth muscle cells (PA-SMC), an effect which depends upon activity of both the 5-HT transporter (5-HTT) and the 5-HT receptors. Expression analysis of lung tissues from PAH patients undergoing lung transplantation revealed an increased expression of the 5-HT transporter (5-HTT) and an enhanced proliferative growth response of isolated pulmonary arterial smooth muscle cells (PASMC) to 5-HT. Serotonin is contained in platelets but is also synthesized by pulmonary endothelial cells which express tryptophan hydroxylase 1, the rate-limiting enzyme of 5-HT synthesis. While inhibitors of 5-HTT and of 5-HT2B receptors can reverse experimental PH, 5-HTT-overexpressing mice spontaneously develop PH. In patients with chronic lung disease, a close association has been found between a 5-HTT gene polymorphism and the severity of pulmonary hypertension. Agents capable of selectively inhibiting 5-HTT-mediated PA-SMC proliferation deserve to be investigated as potential treatments for pulmonary hypertension. However, the 5-HT pathway is still studied only on a preclinical level and the usefulness of drugs interacting with the 5-HT pathway remains to be established in human PAH.
MeSH term(s)	Animals ; Humans ; Hypertension, Pulmonary/etiology ; Receptors, Serotonin/physiology ; Serotonin/physiology ; Serotonin Plasma Membrane Transport Proteins/physiology ; Signal Transduction/physiology
Chemical Substances	Receptors, Serotonin ; Serotonin Plasma Membrane Transport Proteins ; Serotonin (333DO1RDJY)
Language	English
Publishing date	2013
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-642-38664-0_15
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Article ; Online: Telomere attrition in sickle cell anemia.

Mekontso Dessap, Armand / Cecchini, Jérôme / Chaar, Vicky / Marcos, Elisabeth / Habibi, Anoosha / Bartolucci, Pablo / Ghaleh, Bijan / Galacteros, Frederic / Adnot, Serge

American journal of hematology

2017 Volume 92, Issue 6, Page(s) E112–E114

Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Letter
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.24721
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Article ; Online: CCR2/CCR5-mediated macrophage-smooth muscle cell crosstalk in pulmonary hypertension.

Abid, Shariq / Marcos, Elisabeth / Parpaleix, Aurélien / Amsellem, Valérie / Breau, Marielle / Houssaini, Amal / Vienney, Nora / Lefevre, Marine / Derumeaux, Genevieve / Evans, Steven / Hubeau, Cedric / Delcroix, Marion / Quarck, Rozenn / Adnot, Serge / Lipskaia, Larissa

The European respiratory journal

2019 Volume 54, Issue 4

Abstract: Macrophages are major players in the pathogenesis of pulmonary arterial hypertension (PAH).To investigate whether lung macrophages and pulmonary-artery smooth muscle cells (PASMCs) collaborate to stimulate PASMC growth and whether the CCL2-CCR2 and CCL5- ... ...

Abstract	Macrophages are major players in the pathogenesis of pulmonary arterial hypertension (PAH).To investigate whether lung macrophages and pulmonary-artery smooth muscle cells (PASMCs) collaborate to stimulate PASMC growth and whether the CCL2-CCR2 and CCL5-CCR5 pathways inhibited macrophage-PASMC interactions and PAH development, we used human CCR5-knock-in mice and PASMCs from patients with PAH and controls.Conditioned media from murine M1 or M2 macrophages stimulated PASMC growth. This effect was markedly amplified with conditioned media from M2 macrophage/PASMC co-cultures. CCR2, CCR5, CCL2 and CCL5 were upregulated in macrophage/PASMC co-cultures. Compared to inhibiting either receptor, dual CCR2 and CCR5 inhibition more strongly attenuated the growth-promoting effect of conditioned media from M2-macrophage/PASMC co-cultures. Deleting either CCR2 or CCR5 in macrophages or PASMCs attenuated the growth response. In mice with hypoxia- or SUGEN/hypoxia-induced PH, targeting both CCR2 and CCR5 prevented or reversed PH more efficiently than targeting either receptor alone. Patients with PAH exhibited CCR2 and CCR5 upregulation in PASMCs and perivascular macrophages compared to controls. The PASMC growth-promoting effect of conditioned media from M2-macrophage/PASMC co-cultures was greater when PASMCs from PAH patients were used in the co-cultures or as the target cells and was dependent on CCR2 and CCR5. PASMC migration toward M2-macrophages was greater with PASMCs from PAH patients and was attenuated by blocking CCR2 and CCR5.CCR2 and CCR5 are required for collaboration between macrophages and PASMCs to initiate and amplify PASMC migration and proliferation during PAH development. Dual targeting of CCR2 and CCR5 may hold promise for treating human PAH.
MeSH term(s)	Adolescent ; Adult ; Animals ; Cell Communication ; Cell Movement/genetics ; Cell Proliferation/genetics ; Coculture Techniques ; Culture Media, Conditioned ; Disease Models, Animal ; Female ; Gene Knock-In Techniques ; Humans ; Macrophages/metabolism ; Male ; Mice ; Mice, Knockout ; Middle Aged ; Muscle, Smooth, Vascular/cytology ; Muscle, Smooth, Vascular/metabolism ; Myocytes, Smooth Muscle/metabolism ; Pulmonary Arterial Hypertension/genetics ; Pulmonary Arterial Hypertension/metabolism ; Pulmonary Artery/cytology ; Pulmonary Artery/metabolism ; Receptors, CCR2/genetics ; Receptors, CCR2/metabolism ; Receptors, CCR5/genetics ; Receptors, CCR5/metabolism ; Young Adult
Chemical Substances	CCR2 protein, human ; CCR5 protein, human ; CCR5 protein, mouse ; Ccr2 protein, mouse ; Culture Media, Conditioned ; Receptors, CCR2 ; Receptors, CCR5
Language	English
Publishing date	2019-10-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.02308-2018
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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