Michael Ebeid, Ph.D.

Assistant Professor
Downers Grove, IL

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About

Dr. Ebeid is a physician-scientist interested in mammalian cochlear development and regeneration. Dr. Ebeid received his Master Degree in Anatomy and his Medical Degree from Assiut University in Egypt. He received his Doctor of Philosophy in Biomedical Sciences under the mentorship of Dr. Garrett A. Soukup at Creighton University studying the role of Atoh1 transcription factor and microRNA-183 family members in inner ear hair cell development. He continued on to a postdoctoral fellowship at University of Nebraska Medical Center in Omaha, NE under the mentorship of Dr. Sung-Ho Huh studying the role of fibroblast growth factor signaling and Wnt signaling in cochlear development. Dr. Ebeid joined the faculty at Midwestern University in 2019 where he studies novel genes involved in cochlear development and maturation.

Title
Assistant Professor

Campus
Downers Grove, IL

College
College of Graduate Studies - IL

Department
Anatomy

Program
Biomedical Sciences (M.B.S.)
Dental Medicine
Osteopathic Medicine
Physician Assistant Studies

Call My
Office

630-515-6062

Send Me
a Message

mebeid@midwestern.edu

Education

Creighton University | 2016 | Ph.D.
Assiut University | 2009 | M.S.
Assiut University | 2003 | M.B.B.S.

Courses Taught

Lectures on Auditory and Vestibular systems for:

ANATD1521 Neuroscience for Doctor of Osteopathic Medicine (D.O.)

ANATD0565 Neuroscience for Physician Assitant program

IBSSD1521 Neuroscience for Doctor of Dental Medicine (D.M.D.)

ANATD0520 Neuroscience for Master of Biomedical Sciences

Research

About us:

Dr. Ebeid lab is interested in identifying novel genes required for normal development and function of mammalian cochlea. We utilize a variety of mouse genetics, cellular, molecular, imaging and electrophysiological techniques in studying cochlear development and maturation in different genetic mouse models carrying single or multiple gene deletions. Our ultimate goal is to identify novel genes involved in hearing and translate our research into therapeutic techniques to treat hearing loss.

Current members:

Dr. Michael Ebeid, PI

Hongji Zhang, Research Specialist/Lab manager

Amal Yaghmour, MBS-22 student

Gabriele Noreikaite, CCOM-22, student

Kathy Barnas, PT-2024, student

 

Current Projects:

  • Investigate the role of Prdm16 in the development, maturation and function of the cochlea. 

    The PR domain containing 16 (PRDM16) is a key transcription regulator in the development of different tissues including craniofacial, adipose, neural, and hematopoietic tissues. Our lab identified PRDM16 expression in the epithelial cells of the Kölliker’s organ (KO) starting around E13.5 and maintained till the disappearance of the KO around P10. KO undergoes remodeling during development to give rise to the cells of the inner sulcus region and is thought to be involved in tectorial membrane formation as well as generating intrinsic spontaneous activity. This work aims at understanding the role of PRDM16 in cochlear development utilizing loss-of-function approach. Data collected by our lab shows an interesting phenotype in Prdm16-null cochlea including hypoplastic KO, shortened cochlear duct (60% compared to control), increased density of hair cells and supporting cells in the apical turn as well as multiple isolated islands of ectopic hair cells within the KO domain. Ectopic HCs were Sox2+ and Myo6+ with immature stereocilia bundles, and consistent innervation from the spiral ganglion neurons. 

https://anatomypubs.onlinelibrary.wiley.com/doi/10.1002/dvdy.480

  • Identify the impact of ETV transcription factor deletion on the mouse organ of Corti .

The E26 transformation-specific (ETS) proteins are a group of transcription factors with highly conserved DNA binding domain. The PEA3 subgroup includes 3 members: ETV1 , ETV4 and ETV5 which are more than 95% identical in the amino acid sequence within the DNA-binding domain. Our lab has published a paper on the impact of mesenchymal deletion of these 3 factors on the cochlear duct length. Currently, we are investigating the redundant function of these 3 transcription factors in the development and function of supporting cells within the cochlear epithelium. A mouse model with combined deletion of these 3 factors is viable and exhibits a phenotype within the organ of Corti. 

https://www.sciencedirect.com/science/article/pii/S0378595520303105 (Links to an external site.)

  • Characterize distinct subtypes of progenitor cells and their lineages in the developing mouse cochlea.

We have created a dataset of single-cell gene expression profiles of cochlear duct cells at multiple developmental ages and we are currently using bioinformatics and mRNA Fluorescence in-situ hybridization (FISH) to understand the heterogeneity of cochlear duct cells during development. Analysis of enriched genes in populations of progenitor cells as well as lineage tracing of such population will provide better understanding of cochlear development and maturation. 

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  • Generate a novel progenitor cell model to study pharmaceutical agents for hair cell regeneration

With the complexity of inner ear structure, we are in process of creating and validating a novel progenitor cell model to study the progenitor population within the developing cochlea. Genetic mouse model expressing fluorescence protein in progenitor cells is currently used to sort progenitor cells and expand the population in-vitro. Creating such model will facilitate high throughput survey of pharmaceutical compounds application in hair cell regeneration.

If you are interested in joining the lab, please reach out at mebeid@midwestern.edu

Publications

PRDM16 expression and function in mammalian cochlear development. Ebeid M, Barnas K, Zhang H, Yaghmour A, Noreikaite G, Bjork BC. Dev Dyn. 2022 Apr 22. doi: 10.1002/dvdy.480. Epub ahead of print. PMID: 35451126. DOI: 10.1002/dvdy.480

Mesenchymal ETV transcription factors regulate cochlear length. Michael Ebeid, Sung-Ho Huh. Hearing Research, Volume 396, 2020,108039,
ISSN 0378-5955, https://doi.org/10.1016/j.heares.2020.108039. DOI: 10.1016/j.heares.2020.108039

β-Catenin is required for radial cell patterning and identity in the developing mouse cochlea. Lina Jansson, Michael Ebeid, Jessica W. Shen, Tara E. Mokhtari, Lee A. Quiruz, David M. Ornitz, Sung-Ho Huh, Alan G. Cheng. Proceedings of the National Academy of Sciences Sep 2019, 201910223; DOI: https://doi.org/10.1073/pnas.1910223116

FGF signaling: diverse roles during cochlear development. Michael Ebeid, Sung-Ho Huh. BMB reports 2017. DOI: https://doi.org/10.5483/bmbrep.2017.50.10.164

Transcriptome-wide comparison of the impact of Atoh1 and miR-183 family on pluripotent stem cells and multipotent otic progenitor cells. Michael Ebeid, Prashanth Sripal, Jason Pecka, Kirk W. Beisel, Kelvin Kwan, Garrett A. Soukup PLOS ONE July 7, 2017. https://doi.org/10.1371/journal.pone.0180855

 

Organizations

Association for Research in Otolaryngology

https://www.aro.org/

Society For Neuroscience

https://www.sfn.org/

 

 

 

Grants

American Hearing Research Foundation

Mechanism of FGF signaling in regulating mouse cochlear progenitor proliferation

https://www.american-hearing.org/purpose-impact/ahrf-funded-research/grant-recipients/

Midwestern Univeristy (Faculty startup fund 2019)

Midwestern University ORSP outsourcing grant (2020, 2021)