Stefan Heller

Honors and Awards

• McKnight Neuroscience of Brain Disorders Award, McKnight Endowment Fund for Neuroscience (2005-2007)
• Burt Evans Young Investigator Award, National Organization for Hearing Research Foundation (2005)
• Albert and Ellen Grass Faculty Grant Award, Marine Biological Laboratory, Woods Hole, MA (Summer 2004, Summer 2005)
• Franklin M. Rizer Lectureship, The American Neurotology Society (2004)
• Basil O'Connor Starter Scholar Research Award, March of Dimes (2001-2003)

Professional Education

• Postdoctoral Fellow, The Rockefeller University, Sensory Neuroscience (2000)
• Dr rer nat (Ph.D.), Johannes Gutenberg University, Mainz, Germany, Genetics (1994)
• Dipl Biol (M.S.), Johannes Gutenberg University, Mainz, Germany, Biological Sciences (1990)

Postdoctoral Advisees

Christian Grimm, Zhaohua Guo, Meike Herget, Kinuko Masaki, Kazuo Oshima, Veronika Starlinger, Stefan Volkenstein, Zhigang Xu

Graduate & Fellowship Program Affiliations

• Molecular and Cellular Physiology
• Neurosciences

Web Site Links

• Heller Lab Website

Research Interests

Current Lines of Research:

All hearing sensation is derived from the electrical output of a remarkably small number of sensory cells: fewer that 15,000 per cochlea. These hair cells are the mechanoelectrical transducers of the inner ear: deflections of the stereociliary bundles on their apical surfaces lead to transmitter release from their basolateral poles, leading, in turn, to signal generation in the peripheral axons of the auditory nerve fibers.

Most types of congenital and acquired hearing loss arise from loss of these sensory cells. The incidence of heritable deafness is high: one child in a thousand is born deaf; another one in a thousand becomes deaf before adulthood. The prevalence of acquired hearing loss is rising, as the population ages, and as noise pollution steadily increases. It is estimated that one in three adults over the age of 65 has a handicapping hearing loss.

Underlying the irreversibility of hearing loss in mammals is the incapacity to replace lost hair cells by cell division or by regeneration from endogenous cells in the inner ear epithelia. Hair cell replacement, either by stimulation of regeneration (as occurs naturally in non-mammalian vertebrates) or by transplantation of progenitor cells capable of differentiating into hair cells, remains therefore the ultimate goal in the development of treatment applications to reconstruct the damaged inner ear.

Our recent work has focused on creating inner ear cell types, in particular hair cells and auditory neurons, from a renewable source. We have shown that embryonic stem (ES) cells and somatic inner ear stem cells can serve as such a source. The ongoing research in my laboratory is focusing on defining and exploring signaling pathways that control hair cell and auditory neuronal generation in vitro and in vivo toward a better understanding of native inner ear development and, ultimately, to develop cell- or drug-based therapies for inner ear disorders.

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Publications

• Rethinking how hearing happens. Xu Z, Ricci AJ, Heller S "Neuron" 2009 ; 3 (62) : 305-7
• Quo vadis, hair cell regeneration? Brigande JV, Heller S "Nat Neurosci" 2009 ; 6 (12) : 679-685
• MAGI-1, a candidate stereociliary scaffolding protein, associates with the tip-link component cadherin 23. Xu Z, Peng AW, Oshima K, Heller S "J Neurosci" 2008 ; 44 (28) : 11269-76
• Stimulus-specific modulation of the cation channel TRPV4 by PACSIN 3. D'hoedt D, Owsianik G, Prenen J, Cuajungco MP, Grimm C, Heller S, Voets T, Nilius B "J Biol Chem" 2008 ; 10 (283) : 6272-80
• TRP channels as candidates for hearing and balance abnormalities in vertebrates. Cuajungco MP, Grimm C, Heller S "Biochim Biophys Acta" 2007 ; 8 (1772) : 1022-7