Bio

Dr. Julia Abitbol received her B.Sc with Honour's specialization in Biology and Medical Cell Biology at the University of Western Ontario, London, Ontario, Canada. She then received her PhD in Anatomy and Cell Biology at the University of Western Ontario. During her PhD she studied the role of large-pore channel proteins, connexins and pannexins, in the auditory system.

Institute Affiliations

Honors & Awards

  • Suzanne M. Bernier publication Award 2019, The University of Western Ontario (06/2019)
  • Marine Biology Laboratory Travel Award to attend "The Biology of the Inner Ear” workshop, Marine Biology Laboratory (05/2019)
  • Selected Cover Image for Journal of Molecular Medicine, May cover, Journal of Molecular Medicine (05/2019)
  • Feature Platform Presentation Winner, London Health Research Day 2019, London Health Research Day Committee (04/2019)
  • Selected Cover Image Journal of Cell Science, Volume 131, Issue 9, Journal of Cell Science (05/2018)
  • First Author Interview Feature in the Journal of Cell Science, Journal of Cell Science (04/2018)
  • Best Poster Presentation Award, Anatomy and Cell Biology Research Day, Anatomy and Cell Biology Research Day Committee (10/2017)
  • Best Poster Presentation Award, International Gap Junction Meeting, International Gap Junction Meeting Committee (07/2017)
  • Travel Scholarship, International Gap Junction Meeting, International Gap Junction Meeting Organizing Committee (07/2017)
  • Natural Sciences and Engineering Research Council (NSERC) CGS Doctoral Scholarship, Natural Sciences and Engineering Research Council (09/2017-11/2019)
  • Ontario Graduate Scholarship (Declined), The University of Western Ontario (09/2017-08/2018)
  • Ontario Graduate Scholarship, The University of Western Ontario (09/2016-04/2017)
  • JAX Lab Mouse Research Travel Scholarship, JAX Lab, Bar Harbour, Maine (09/2016)
  • Anatomy and Cell Biology Travel Award, The Department of Anatomy and Cell Biology, The University of Western Ontario (04/2016)
  • Western Graduate Research Scholarship, The University of Western Ontario (09/2014-08/2019)

Professional Education

  • Bachelor of Science, Unlisted School (2014)
  • Doctor of Philosophy, Unlisted School (2019)
  • Bachelor of Science, The University of Western Ontario, Honors Specialization in Biology and Medical Cell Biology (2014)
  • Doctor of Philosophy, The University of Western Ontario, Anatomy and Cell Biology (2019)

Stanford Advisors

Contact

  • Academic
    jabitbol@stanford.edu
    University - Scholar Department: OHNS/Otolaryngology/Head & Neck Surgery Position: Postdoctoral Scholar

Additional Info

  • Mail Code: 5365

Links

Current Research and Scholarly Interests

Hearing loss is one of the most common sensory deficits and is permanent. We have known for quite some time that avian species retain the ability to spontaneously regenerate hair cells when they are damaged, however, this does not occur in the adult mammalian cochlea. My research interests are to enhance the proliferative regeneration capacity of the mammalian cochlea by findings genes that may up-regulate this process. Further, my goal is to track the dynamics of proliferating cochlear cells after damage in the cochlear. The ultimate goal is to identify genes that may enhance spontaneous regeneration of cochlear cells upon damage to treat patients with hearing loss.

All Publications

  • Hair Cell Regeneration: From Animals to Humans. Clinical and experimental otorhinolaryngology Choi, S. W., Abitbol, J., Cheng, A. 2024

    Abstract

    Cochlear hair cells are critical in converting sound into electrical signals that are relayed via the spiral ganglion neurons to the central auditory pathway. Hair cells are vulnerable to damage caused by excessive noise, aging, and ototoxic agents. Non-mammals can regenerate lost hair cells by mitotic regeneration and direct transdifferentiation of surrounding supporting cells. However, in mature mammals, damaged hair cells are not replaced, resulting in permanent hearing loss. Recent studies have uncovered mechanisms by which sensory organs in non-mammals and the neonatal mammalian cochlea regenerate hair cells, and outlined possible mechanisms why this ability declines rapidly with age in mammals. Here, we review similarities and differences between avian, zebrafish and mammalian hair cell regeneration. Moreover, we discuss advances and limitations of hair cell regeneration in the mature cochlea and their potential applications to human hearing loss.

    View details for DOI 10.21053/ceo.2023.01382

    View details for PubMedID 38271988

  • Selection of viral capsids and promoters affects the efficacy of rescue of Tmprss3-deficient cochlea. Molecular therapy. Methods & clinical development Aaron, K. A., Pekrun, K., Atkinson, P. J., Billings, S. E., Abitbol, J. M., Lee, I. A., Eltawil, Y., Chen, Y. S., Dong, W., Nelson, R. F., Kay, M. A., Cheng, A. G. 2023; 30: 413-428

    Abstract

    Adeno-associated virus (AAV)-mediated gene transfer has shown promise in rescuing mouse models of genetic hearing loss, but how viral capsid and promoter selection affects efficacy is poorly characterized. Here, we tested combinations of AAVs and promoters to deliver Tmprss3, mutations in which are associated with hearing loss in humans. Tmprss3tm1/tm1 mice display severe cochlear hair cell degeneration, loss of auditory brainstem responses, and delayed loss of spiral ganglion neurons. Under the ubiquitous CAG promoter and AAV-KP1 capsid, Tmprss3 overexpression caused striking cytotoxicity in vitro and in vivo and failed to rescue degeneration or dysfunction of the Tmprss3tm1/tm1 cochlea. Reducing the dosage or using AAV-DJ-CAG-Tmprss3 diminished cytotoxicity without rescue of the Tmprss3tm1/tm1 cochlea. Finally, the combination of AAV-KP1 capsid and the EF1α promoter prevented cytotoxicity and reduced hair cell degeneration, loss of spiral ganglion neurons, and improved hearing thresholds in Tmprss3tm1/tm1 mice. Together, our study illustrates toxicity of exogenous genes and factors governing rescue efficiency, and suggests that cochlear gene therapy likely requires precisely targeted transgene expression.

    View details for DOI 10.1016/j.omtm.2023.08.004

    View details for PubMedID 37663645

    View details for PubMedCentralID PMC10471831

  • Lineage-tracing and translatomic analysis of damage-inducible mitotic cochlear progenitors identifies candidate genes regulating regeneration. PLoS biology Udagawa, T., Atkinson, P. J., Milon, B., Abitbol, J. M., Song, Y., Sperber, M., Huarcaya Najarro, E., Scheibinger, M., Elkon, R., Hertzano, R., Cheng, A. G. 2021; 19 (11): e3001445

    Abstract

    Cochlear supporting cells (SCs) are glia-like cells critical for hearing function. In the neonatal cochlea, the greater epithelial ridge (GER) is a mitotically quiescent and transient organ, which has been shown to nonmitotically regenerate SCs. Here, we ablated Lgr5+ SCs using Lgr5-DTR mice and found mitotic regeneration of SCs by GER cells in vivo. With lineage tracing, we show that the GER houses progenitor cells that robustly divide and migrate into the organ of Corti to replenish ablated SCs. Regenerated SCs display coordinated calcium transients, markers of the SC subtype inner phalangeal cells, and survive in the mature cochlea. Via RiboTag, RNA-sequencing, and gene clustering algorithms, we reveal 11 distinct gene clusters comprising markers of the quiescent and damaged GER, and damage-responsive genes driving cell migration and mitotic regeneration. Together, our study characterizes GER cells as mitotic progenitors with regenerative potential and unveils their quiescent and damaged translatomes.

    View details for DOI 10.1371/journal.pbio.3001445

    View details for PubMedID 34758021

  • GJB2 mutations linked to hearing loss exhibit differential trafficking and functional defects as revealed in cochlear-relevant cells Frontiers in Cell and Development Biology Beach, R., Abitbol, J. M., Allman, B. L., Esseltine, J. L., Shao, Q., Laird, D. W. 2020; 8 (215)

    View details for DOI 10.3389/fcell.2020.00215

  • Cisplatin-induced ototoxicity occurs independent of gap junctional intercellular communication, in press Cell Death and Differentiation Abitbol, J. M., Beach, R., Esseltine, J. L., Barr, K., Allman, B. L., Laird, D. W. 2020
  • The connexin 30 A88V mutant reduces cochlear gap junction expression and confers long-term protection against hearing loss The Journal of Cell Science Kelly, J. J., Abitbol, J. M., Hulme, S., Pree, E. R., Laird, D. W., Allman, B. L. 2019; 132 (2)

    View details for DOI 10.1242/jcs.224097

  • Double deletion of Panx1 and Panx3 affects skin and bone but not hearing Journal of Molecular Medicine Abitbol, J. M., O'Donnell, B. L., Wakefield, B. C., Jewel, E., Kelly, J. J., Barr, K. J., Willmore, K. E., Penuela, S. 2019; 97 (5): 723-736

    View details for DOI 10.1007/s00109-019-01779-9

  • Mice harbouring an oculodentodigital dysplasia-linked Cx43 G60S mutation have severe hearing loss. The Journal of Cell Science Abitbol, J. M., Kelly, J. J., Barr, K. J., Allman, B. L., Laird, D. W. 2018; 131

    View details for DOI 10.1242/jcs.214635

  • Differential effects of pannexins on noise-induced hearing loss Biochemical Journal Abitbol, J. M., Kelly, J. J., Barr, K., Schormans, A. L., Laird, D. W., Allman, B. L. 2016; 473 (24): 4665-4680

    View details for DOI 10.1042/BCJ20160668