WorldCat Identities

Guinamard, Romain

Works: 6 works in 8 publications in 2 languages and 10 library holdings
Roles: Other, Thesis advisor, Opponent
Classifications: R1, 616.1
Publication Timeline
Most widely held works by Romain Guinamard
Variabilité glycémique : exploration in vitro des fonctions cellulaires et mitochondriales sur la lignée de cardiomyocyte HL-1 by Patrick Mordel( Book )

2 editions published in 2017 in French and held by 2 WorldCat member libraries worldwide

Le diabète est associé à une augmentation de risque de maladie cardiovasculaire et une dérégulation du métabolisme. Il a été suggéré que la variabilité glycémique (VG) pouvait avoir un rôle dans le développement des complications du diabète. Afin d'étudier et de caractériser les dysfonctions induites par la VG, nous avons mis au point un modèle in vitro mimant la VG sur la lignée de cardiomyocytes HL-1. Nous avons ainsi développé un traitement de 12 heures, mimant hypoglycémie, normoglycémie, hyperglycémie et VG. L'étude de la signalisation cellulaire ne nous a pas permis de montrer un rôle délétère de la VG. Nous avons toutefois mis en évidence que la VG participait à des dysfonctions mitochondriales. En effet en situation de fluctuations en glucose, les mitochondries des cellules HL-1 présentent une augmentation de leur potentiel de membrane, ainsi qu'une augmentation de la production d'anions superoxydes. Bien que nous n'ayons pas réussi à montrer de perturbation de la chaîne respiratoire après 12 heures d'exposition, nous avons pu montrer que 72 heures d'exposition provoquaient une baisse de la respiration mitochondriale. Nous avons enfin étudié l'impact des fluctuations en glucose sur la susceptibilité au développement de lésions d'hypoxie, et avons montré que les lésions sont majorées après 36 heures d'hypoxie en cas d'exposition à des fluctuations en glucose. Nos résultats montrent un rôle délétère de la VG, néanmoins des expériences complémentaires sont nécessaires afin de caractériser de manière plus précise les mécanismes impliqués
TRPM4 non-selective cation channel variants in long QT syndrome by Thomas Hof( )

1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide

Caractérisation fonctionnelle et moléculaire du courant cationique non selectif activé par le calcium sur les cellules sinusales et auriculaires de mammifères by Marie Demion( Book )

2 editions published in 2006 in French and held by 2 WorldCat member libraries worldwide

Recent studies, on cardiac tissue at the ventricular level, showed in pathological conditions the expression of a calcium-activated nonselective cationic channel (NSCCa) supposed to be implicated in the genesis of arrhythmias. The aim of the present study was to search for this current on other cardiac levels: atria and sino-atrial nodes. Using the inside-out configuration of the patch-clamp technique, we showed the presence, on human atrial cardiomyocytes and mouse SAN cells, of a nonselective cationic current, permeable to monovalents cations but impermeable to divalents cations and anions. The current/voltage relationship is linear with a unitary conductance close to 20 pS. This current is activated by rise of intracellular calcium and membrane depolarization but inhibited by internal ATP. It is blocked by flufenamic acid and glibenclamide. This current probably corresponds to the new cloned protein TRPM4, which shares the same electrophysiological properties. We detected its mRNA transcript on human atrium and mouse SAN tissues and its protein on mouse SAN tissue. If the physiological impact of this channel is unclear, it could be implicated on arrhythmias genesis during ischemia. As the calcium/ATP ratio is increased and then is in favour of its activation. Also, we described at the unitary level on human atrial cardiomyocytes, a new chloride current activated by cell swelling so called ICl.swell. It could be implicated in the regulatory volume decrease observed during atrial dilatation
Transient receptor potential channels in cardiac health and disease by Thomas Hof( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Effets de l'étirement axial sur des cardiomyocytes murins déficients en dystrophine : dérégulation calcique et canaux TRPs by Elizabeth Aguettaz( )

1 edition published in 2015 in French and held by 1 WorldCat member library worldwide

Duchenne muscular dystrophy (DMD) is the consequence of the loss of dystrophin, a subsarcolemmal protein essential for mechanical and functional maintenances of the sarcolemma. This deficiency could increase cationic influxes by membrane microruptures or by dysregulation of channels such as stretch-activated channels (SACs). In this work, the effects of a mechanical stretch were explored on cardiomyocytes in the pathological context of dilated cardiomyopathy associated with DMD. Using carbon fibers, an homogenous axial stretch was performed to mimic physiological conditions of ventricular filling. In these conditions, exploration of membrane topography using the scanning ion conductance microscopy did not show any surface evolution or sarcolemma disruption in stretch condition. The study was thus focused on activity and identification of molecular candidates for SACs, especially the TRPs (Transient Receptor Potential) channels in the stretch-induced. Ca2+ homeostasis dysregulation. Cationic influxes assessed by Mn2+-quenching and assessment of the intracellular Ca2+ concentration ([Ca2+]i) using fluo-8 fluorescence demonstrated an involvement of TRPV2 and TRPCs channels. The first ones seem to be responsible for cationic entry and [Ca2+]i increase in mdx cardiomyocytes. The latter, though responsible for an influx, do not contribute to [Ca2+]i increase. These findings reveal that TRPV2 channels could play an important role in calcium dysregulation observed in dystrophin-deficient cardiomyocytes
Le canal calcique Orai1 : nouvel acteur impliqué dans la physiopathologie cardiaque by Fiona Bartoli( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

While the SOCE (store-operated Ca2+ entry), carried by TRPCs (transient receptor potential canonical) and Orai1 channels, is essential in non-excitable cells, its physiological role in adult cardiomyocytes remains elusive. Nevertheless, it is well established that exacerbated TRPCs/STIM1-dependent Ca2+ entry participates in the pathogenesis of hypertrophy and heart failure (HF) via the induction of pro-hypertrophic signaling pathways, such as CaMKII (Ca2+/calmodulin-kinase II) and calcineurin (CaN)/ NFAT (nuclear factor of activated T-cells). By contrast, functional inhibition or gene silencing of TRPCs and STIM1 is cardioprotective against hypertrophic insults. As for Orai1 Ca2+ channels, their pathophysiological roles in the heart remain unknown and under debate, since in vitro Orai1 silencing has a beneficial effect against cardiomyocyte hypertrophy, whereas in vivo silencing has deleterious effects with the development of dilated cardiomyopathy. Further investigations are necessary to determine the pathophysiological role of Orai1 in the heart. My thesis objectives are to explore the role of Orai1-dependent Ca2+ signaling in the heart under physiological and pathological conditions using a transgenic mouse model expressing a non functional mutant of Orai1, specifically in the heart (dn-Orai1R91W/tTa) and a selective pharmacological inhibitor, JPIII. First, we showed that dn-Orai1R91W/tTa mice have normal cardiac function and conserved Ca2+ homeostasis involved in the excitation-contraction coupling suggesting that Orai1 is not instrumental in regulating cardiac function under physiological conditions. However, we demonstrated an increased Orai1 expression and activity in a mouse model of cardiac hypertrophy induced by pressure overload, which is a maladaptive alteration involved in pathological ventricular dysfunction. By contrast, functional inhibition of Orai1 by genetic manipulation or by the pharmacological tool (JPIII) protects the heart from ventricular dysfunction after pressure overload-induced cardiac hypertrophy. This beneficial effect is related to a restoration of Ca2+ homeostasis and more specifically, is due to preserved ATPase SERCA2a pump expression. We also showed that the aldosterone/mineralocorticoid receptor signaling pathway modulates the expression of TRPC1, -C4, -C5 channels and also the Orai1 channels expression via the SGK1 (Serum and Glucocorticoid-regulated Kinase 1) protein, in neonatal rat ventricular cardiomyocytes. The activation of this signaling pathway could be the cause of the TRPCs/Orai1 channels overexpression found during cardiac hypertrophy. In conclusion, our studies highlighted that Orai1 Ca2+ channels could constitute potential therapeutic target in the treatment of cardiac hypertrophy and HF
Audience Level
Audience Level
  General Special  
Audience level: 0.96 (from 0.93 for Caractéri ... to 0.99 for Le canal c ...)

Alternative Names
Romain Guinamard onderzoeker