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  6. Cardiovascular Axis: Jean-Luc Balligand Research Group

Cardiovascular Axis: Jean-Luc Balligand Research Group

J-L Balligand and his team developed the core of their research projects in the biochemistry and cellular biology of nitric oxide synthases (NOS) including their regulation in cardiovascular tissues. His group initiated the research on the role of NOS in cardiac myocyte contractility which is being extended in the context of myocardial remodelling and regeneration, e.g. in response to neurohormones and adrenoceptors. His lab has recognized expertise in cell signalling and cardiovascular pharmacology using in vitro and in vivo models. JL Balligand is Head of the FATH Pole within IREC and also practicing Physician at the Cliniques Universitaires Saint-Luc, UCL and teaches cardiovascular physiology and pharmacology at UCL Medical School.

More recently, JL Balligand has developed these research directions as associated partner of a Leducq Foundation-funded transatlantic network of excellence in cardiovascular sciences ( http://www.leducq-transatlantic-network.org ) and of of the FP6-EUGeneHeart consortium ( http://www.eugneheart.eu ) that laid the ground for innovative research in therapeutics for heart failure. He also coordinates several collaborative programmes (Concerted Actions, Interuniversity Attraction Pole) funded by the Politique Scientifique Fédérale. He is the coordinator of the Clinical Trial “Beta3_LVH” (www.beta3lvh.eu) that is currently testing the effect of the beta3 adrenergic agonist, mirabegron for the prevention of heart failure with preserved ejection fraction. (funded by a European Commission Horizon2020 grant).

J-L Balligand is a Board member of the ESC Council on Basic Cardiovascular Science and has been co-director of the Summer School in Basic Cardiovascular Research sponsored by the Council since 2009. Since September 2009, Prof Balligand is also Board member of BioWin ( http://www.biowin.org ), the Health Sciences cluster of Wallonia that promotes translational innovative research in partnership with biomedical industries (cfr. Insight in Nature, Sept 6, 2012).

Brief list of publications of the group

Dnmt3a-mediated inhibition of Wnt in cardiac progenitor cells improves differentiation and remote remodeling after infarction.

De Pauw A, Andre E, Sekkali B, Bouzin C, Esfahani H, Barbier N, Loriot A, De Smet C, Vanhoutte L, Moniotte S, Gerber B, di Mauro V, Catalucci D, Feron O, Hilfiker-Kleiner D, Balligand JL.

JCI Insight. 2017 ;2(12).

Cardiac myocyte b3-adrenergic receptors prevent myocardial fibrosis by modulating oxidant stress-dependent paracrine signaling.

Hermida N, Michel L, Esfahani H, Dubois-Deruy E, Hammond J, Bouzin C, Markl A, Colin H, Van Steenbergen A, De Meester C, Beauloye C, Horman S, Yin X, Mayr M, Balligand JL.

European Heart Journal; 2017 0, 1-11

Paracrine nitric oxide induces expression of cardiac sarcomeric proteins in adult progenitor cells through soluble guanylyl cyclase/cyclic-guanosine monophosphate and Wnt/β-catenin inhibition.

De Pauw A, Massion P, Sekkali B, Andre E, Dubroca C, Kmecova J, Bouzin C, Friart A, Sibille C, Gilon P, De Mulder D, Esfahani H, Strapart A, Martherus R, Payen V, Sonveaux P, Brouckaert P, Janssens S, Balligand JL. 

Cardiovasc Res. 2016 Oct;112(1):478-90. doi: 10.1093/cvr/cvw196.

 

Enhanced expression of β3-adrenoceptors in cardiac myocytes attenuates neurohormone-induced hypertrophic remodeling through nitric oxide synthase.

Belge C, Hammond J, Dubois-Deruy E, Manoury B, Hamelet J, Beauloye C, Markl A, Pouleur AC, Bertrand L, Esfahani H, Jnaoui K, Götz KR, Nikolaev VO, Vanderper A, Herijgers P, Lobysheva I, Iaccarino G, Hilfiker-Kleiner D, Tavernier G, Langin D, Dessy C, Balligand JL. 

Circulation. 2014 Jan 28;129(4):451-62. doi: 10.1161/CIRCULATIONAHA.113.004940.

 

Nitric oxide synthase and cyclic GMP signaling in cardiac myocytes: from contractility to remodeling.

Hammond J, Balligand JL.

J Mol Cell Cardiol. 2012 Feb;52(2):330-40. doi: 10.1016/j.yjmcc.2011.07.029. Review.

 

Endogenous nitric oxide mechanisms mediate the stretch dependence of Ca2+ release in cardiomyocytes.

Petroff MG, Kim SH, Pepe S, Dessy C, Marbán E, Balligand JL, Sollott SJ.

Nat Cell Biol. 2001 Oct;3(10):867-73.

Upregulation of beta(3)-adrenoceptors and altered contractile response to inotropic amines in human failing myocardium.

Moniotte S, Kobzik L, Feron O, Trochu JN, Gauthier C, Balligand JL.

Circulation. 2001 Mar 27;103(12):1649-55.