Myo/Nog cells: A Novel Approach to Neuroprotection in the Retina

Arturo Bravo Nuevo; Mindy George-Weinstein; Jacquelyn Gerhart; Alexa Noel McGrath; Samantha Murad; Paul Lecker; Karanveer Johal; John Spikes; Jonathan Stone; Alice Brandill; Diana Crowley; Rushil Brahmbhatt; Christopher Sutera; Jake Bernstein; Nathan Morrison

doi:/article.aspx?articleid=2767563resultClick=1

Myo/Nog cells: A Novel Approach to Neuroprotection in the Retina

Arturo Bravo Nuevo, Mindy George-Weinstein, Jacquelyn Gerhart, Alexa Noel McGrath, Samantha Murad, Paul Lecker, Karanveer Johal, John Spikes, Jonathan Stone, Alice Brandill, Diana Crowley, Rushil Brahmbhatt, Christopher Sutera, Jake Bernstein, Nathan Morrison

Research output: Contribution to conference › Presentation

Abstract

 Purpose : Myo/Nog cells, named for their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin, are critical regulators of embryonic development, including eye morphogenesis. In the normal adult eye, Myo/Nog cells are present in low numbers throughout the anterior and posterior segments. Here we study the behaviors of Myo/Nog cells in different models of retinal stress and degeneration.
 
 Methods : The numbers and distribution of Myo/Nog cells and cell death were determined by immunofluorescence microscopy in the following models: 1) the critical period of physiological culling of photoreceptors, 2) hypoxia induced cell death, 3) light damage, 4) genetically induced retinal degeneration, and 5) increased intraocular pressure. Optical coherence tomography and electroretinography were used to imagine the retina and measure visual function, respectively.
 
 Results : Myo/Nog cells increase in number and migrate to areas of stress and cell death in the retina. Depletion of Myo/Nog cells leads to increased neuronal cell damage. Addition of exogenous Myo/Nog cells significantly reduces neuronal cell death and improves visual function.
 
 Conclusions : Myo/Nog cells are highly responsive to a perturbation in retinal homeostasis induced by different forms of stress and injury. Myo/Nog cells are neuroprotective under these conditions. However, their capacity to differentiate into myofibroblasts must be taken into account when considering an approach of Myo/Nog cell based therapy.
 
 This is a 2020 ARVO Annual Meeting abstract.

Original language	American English
DOIs	https://doi.org//article.aspx?articleid=2767563resultClick=1
State	Published - Jun 2020
Event	ARVO 2020 Annual Meeting - Baltimore, MD Duration: Jun 1 2020 → …

Conference

Conference	ARVO 2020 Annual Meeting
Period	6/1/20 → …

Disciplines

Medicine and Health Sciences
Ophthalmology

Access to Document

/article.aspx?articleid=2767563resultClick=1License: Unspecified

Cite this

Bravo Nuevo, A., George-Weinstein, M., Gerhart, J., McGrath, A. N., Murad, S., Lecker, P., Johal, K., Spikes, J., Stone, J., Brandill, A., Crowley, D., Brahmbhatt, R., Sutera, C., Bernstein, J., & Morrison, N. (2020). Myo/Nog cells: A Novel Approach to Neuroprotection in the Retina. ARVO 2020 Annual Meeting. https://doi.org//article.aspx?articleid=2767563resultClick=1

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abstract = " Purpose : Myo/Nog cells, named for their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin, are critical regulators of embryonic development, including eye morphogenesis. In the normal adult eye, Myo/Nog cells are present in low numbers throughout the anterior and posterior segments. Here we study the behaviors of Myo/Nog cells in different models of retinal stress and degeneration. Methods : The numbers and distribution of Myo/Nog cells and cell death were determined by immunofluorescence microscopy in the following models: 1) the critical period of physiological culling of photoreceptors, 2) hypoxia induced cell death, 3) light damage, 4) genetically induced retinal degeneration, and 5) increased intraocular pressure. Optical coherence tomography and electroretinography were used to imagine the retina and measure visual function, respectively. Results : Myo/Nog cells increase in number and migrate to areas of stress and cell death in the retina. Depletion of Myo/Nog cells leads to increased neuronal cell damage. Addition of exogenous Myo/Nog cells significantly reduces neuronal cell death and improves visual function. Conclusions : Myo/Nog cells are highly responsive to a perturbation in retinal homeostasis induced by different forms of stress and injury. Myo/Nog cells are neuroprotective under these conditions. However, their capacity to differentiate into myofibroblasts must be taken into account when considering an approach of Myo/Nog cell based therapy. This is a 2020 ARVO Annual Meeting abstract.",

author = "{Bravo Nuevo}, Arturo and Mindy George-Weinstein and Jacquelyn Gerhart and McGrath, {Alexa Noel} and Samantha Murad and Paul Lecker and Karanveer Johal and John Spikes and Jonathan Stone and Alice Brandill and Diana Crowley and Rushil Brahmbhatt and Christopher Sutera and Jake Bernstein and Nathan Morrison",

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T1 - Myo/Nog cells: A Novel Approach to Neuroprotection in the Retina

AU - Bravo Nuevo, Arturo

AU - George-Weinstein, Mindy

AU - Gerhart, Jacquelyn

AU - McGrath, Alexa Noel

AU - Murad, Samantha

AU - Lecker, Paul

AU - Johal, Karanveer

AU - Spikes, John

AU - Stone, Jonathan

AU - Brandill, Alice

AU - Crowley, Diana

AU - Brahmbhatt, Rushil

AU - Sutera, Christopher

AU - Bernstein, Jake

AU - Morrison, Nathan

PY - 2020/6

Y1 - 2020/6

N2 - Purpose : Myo/Nog cells, named for their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin, are critical regulators of embryonic development, including eye morphogenesis. In the normal adult eye, Myo/Nog cells are present in low numbers throughout the anterior and posterior segments. Here we study the behaviors of Myo/Nog cells in different models of retinal stress and degeneration. Methods : The numbers and distribution of Myo/Nog cells and cell death were determined by immunofluorescence microscopy in the following models: 1) the critical period of physiological culling of photoreceptors, 2) hypoxia induced cell death, 3) light damage, 4) genetically induced retinal degeneration, and 5) increased intraocular pressure. Optical coherence tomography and electroretinography were used to imagine the retina and measure visual function, respectively. Results : Myo/Nog cells increase in number and migrate to areas of stress and cell death in the retina. Depletion of Myo/Nog cells leads to increased neuronal cell damage. Addition of exogenous Myo/Nog cells significantly reduces neuronal cell death and improves visual function. Conclusions : Myo/Nog cells are highly responsive to a perturbation in retinal homeostasis induced by different forms of stress and injury. Myo/Nog cells are neuroprotective under these conditions. However, their capacity to differentiate into myofibroblasts must be taken into account when considering an approach of Myo/Nog cell based therapy. This is a 2020 ARVO Annual Meeting abstract.

AB - Purpose : Myo/Nog cells, named for their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin, are critical regulators of embryonic development, including eye morphogenesis. In the normal adult eye, Myo/Nog cells are present in low numbers throughout the anterior and posterior segments. Here we study the behaviors of Myo/Nog cells in different models of retinal stress and degeneration. Methods : The numbers and distribution of Myo/Nog cells and cell death were determined by immunofluorescence microscopy in the following models: 1) the critical period of physiological culling of photoreceptors, 2) hypoxia induced cell death, 3) light damage, 4) genetically induced retinal degeneration, and 5) increased intraocular pressure. Optical coherence tomography and electroretinography were used to imagine the retina and measure visual function, respectively. Results : Myo/Nog cells increase in number and migrate to areas of stress and cell death in the retina. Depletion of Myo/Nog cells leads to increased neuronal cell damage. Addition of exogenous Myo/Nog cells significantly reduces neuronal cell death and improves visual function. Conclusions : Myo/Nog cells are highly responsive to a perturbation in retinal homeostasis induced by different forms of stress and injury. Myo/Nog cells are neuroprotective under these conditions. However, their capacity to differentiate into myofibroblasts must be taken into account when considering an approach of Myo/Nog cell based therapy. This is a 2020 ARVO Annual Meeting abstract.

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