Benoit Bruneau, PhD

Professor
Department of Pediatrics
+1 415 734-2708
Research Description: 

The main focus of our lab is to understand how a heart becomes a heart: what cell lineage decisions take place to direct cardiac differentiation, and what morphogenetic and patterning processes occur to assemble all of the heart's components into a functional organ. We are primarily interested in regulation of these processes by transcriptional regulatory mechanisms that include DNA-binding transcription factors, chromatin remodeling complexes, and histone modifications. We have used this knowledge to understand disease mechanisms, but also to devise strategies for cardiac regeneration.

Why study heart development? We believe that primary defects in patterning in early heart development are at the root of congenital heart defects, which affect approximately 1% of live-born children, and we want to understand how these defects occur, to perhaps be able to uncover new and improved diagnostic or even therapeutic options. Also, by understanding how cardiac lineage specification occurs, we can better design stem cell-based interventions of cardiac repair, based on the knowledge of what drives an uncommitted cell towards a specific cardiac fate. We have recently focused our efforts on cardiac chromatin remodeling and modification factors, enzymes that unwind DNA or modify histones to turn genes on or off. We are particularly interested in how these factors control cardiac cell lineage decisions. These chromatin remodeling factors may also be key to pushing a stem cell into becoming a heart cell, perhaps opening up new avenues for cardiac regenerative medicine.

Primary Thematic Area: 
Developmental & Stem Cell Biology
Secondary Thematic Area: 
Vascular & Cardiac Biology
Research Summary: 
Transcriptional regulation of cardiac morphogenesis and differentiation
Publications: 

Author Correction: Transcriptional profiling and therapeutic targeting of oxidative stress in neuroinflammation.

Nature immunology

Mendiola AS, Ryu JK, Bardehle S, Meyer-Franke A, Ang KK, Wilson C, Baeten KM, Hanspers K, Merlini M, Thomas S, Petersen MA, Williams A, Thomas R, Rafalski VA, Meza-Acevedo R, Tognatta R, Yan Z, Pfaff SJ, Machado MR, Bedard C, Coronado PER, Jiang X, Wang J, Pleiss MA, Green AJ, Zamvil SS, Pico AR, Bruneau BG, Arkin MR, Akassoglou K

Author Correction: Defining the relative and combined contribution of CTCF and CTCFL to genomic regulation.

Genome biology

Nishana M, Ha C, Rodriguez-Hernaez J, Ranjbaran A, Chio E, Nora EP, Badri SB, Kloetgen A, Bruneau BG, Tsirigos A, Skok JA

Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling.

The Journal of clinical investigation

Hsu A, Duan Q, McMahon S, Huang Y, Wood SA, Gray NS, Wang B, Bruneau BG, Haldar SM

Cardiac natriuretic peptides.

Nature reviews. Cardiology

Goetze JP, Bruneau BG, Ramos HR, Ogawa T, de Bold MK, de Bold AJ

Defining the relative and combined contribution of CTCF and CTCFL to genomic regulation.

Genome biology

Nishana M, Ha C, Rodriguez-Hernaez J, Ranjbaran A, Chio E, Nora EP, Badri SB, Kloetgen A, Bruneau BG, Tsirigos A, Skok JA