Myo/Nog Cells Migrate to Areas of Stress within The Eye in a Mouse Model of Glaucoma

Paul Lecker; Karnaveer Johal; John Spikes; Jake Bernstein; Alexa Noel McGrath; Victoria MacPherson; Rushil Brahmbhatt; Mark Martin; Christopher Sutera; Brent Biscoe; Jashanveer Johal; Jacquelyn Gerhart; Grzegorz Gorski; Mindy George-Weinstein; Arturo Bravo Nuevo

doi:/article.aspx?articleid=2766662

Myo/Nog Cells Migrate to Areas of Stress within The Eye in a Mouse Model of Glaucoma

Paul Lecker, Karnaveer Johal, John Spikes, Jake Bernstein, Alexa Noel McGrath, Victoria MacPherson, Rushil Brahmbhatt, Mark Martin, Christopher Sutera, Brent Biscoe, Jashanveer Johal, Jacquelyn Gerhart, Grzegorz Gorski, Mindy George-Weinstein, Arturo Bravo Nuevo

Research output: Contribution to conference › Presentation

Abstract

 Purpose : Myo/Nog cells were discovered in the early embryo by their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenic protein inhibitor noggin. Their release of noggin is critical for normal embryonic development, including eye morphogenesis. Myo/Nog cells also are present in the adult eye where they respond to stress and injury. Depletion of Myo/Nog cells was associated with increased photoreceptor cell death, while their addition to the vitreous preserved function and reduced cell death following light damage. The goal of this project was to examine the behavior of Myo/Nog cells in response to increased intraocular pressure (IOP) and subsequent retinal damage in a mouse model of glaucoma.
 
 Methods : The right eyes of C57BL/6J mice were injected with 2µL of microbeads into the anterior chamber to reduce outflow of aqueous humor and induce a glaucomatous state. IOP was measured prior to bead injection and 4, 7 and 21 days after injection. Optical coherence tomography (OCT) was used to image the retina 2 days prior to Glaucoma induction and also 2 days prior to culling. [ABN1] Eyes were collected at D25. The number and location of endogenous Myo/Nog cells were determined by immunofluorescence microscopy. Retinal ganglion cell layer (RGC) and nerve fiber layer (NFL) thickness was further analyzed histologically. Myo/Nog cells isolated from the brain were injected into the anterior chamber to determine their ability to integrate into issues and home to areas of stress.
 
 Results : OCT revealed increased optic cup/disk asymmetry and depth, and decreased RGC/NFL thickness after induction of glaucoma. Endogenous Myo/Nog cells were increased around the optic nerve and periphery of the retina compared to normal retinas. Myo/Nog cells injected into the anterior chamber were tracked to areas of stress such as the trabecular meshwork, the ciliary body and the canal of Schlemm.
 
 Conclusions : Consistent with our previous studies in other models of retinopathy, Myo/Nog cells increase in number in response to elevated IOP and are concentrated in areas of stress in the retina. Myo/Nog cells injected into the anterior chamber revealed become integrated into tissues that are affected by impaired aqueous humor outflow. The impact of Myo/Nog cells on retinal damage induced by glaucoma is under investigation.
 
 This is a 2020 ARVO Annual Meeting abstract.

Original language	American English
DOIs	https://doi.org//article.aspx?articleid=2766662
State	Published - Jun 2020
Event	ARVO Annual Meeting 2020 - Honolulu, Hawaii Duration: Jun 1 2020 → …

Conference

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

Disciplines

Medicine and Health Sciences
Ophthalmology

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Cite this

Lecker, P., Johal, K., Spikes, J., Bernstein, J., McGrath, A. N., MacPherson, V., Brahmbhatt, R., Martin, M., Sutera, C., Biscoe, B., Johal, J., Gerhart, J., Gorski, G., George-Weinstein, M., & Bravo Nuevo, A. (2020). Myo/Nog Cells Migrate to Areas of Stress within The Eye in a Mouse Model of Glaucoma. ARVO Annual Meeting 2020. https://doi.org//article.aspx?articleid=2766662

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abstract = " Purpose : Myo/Nog cells were discovered in the early embryo by their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenic protein inhibitor noggin. Their release of noggin is critical for normal embryonic development, including eye morphogenesis. Myo/Nog cells also are present in the adult eye where they respond to stress and injury. Depletion of Myo/Nog cells was associated with increased photoreceptor cell death, while their addition to the vitreous preserved function and reduced cell death following light damage. The goal of this project was to examine the behavior of Myo/Nog cells in response to increased intraocular pressure (IOP) and subsequent retinal damage in a mouse model of glaucoma. Methods : The right eyes of C57BL/6J mice were injected with 2µL of microbeads into the anterior chamber to reduce outflow of aqueous humor and induce a glaucomatous state. IOP was measured prior to bead injection and 4, 7 and 21 days after injection. Optical coherence tomography (OCT) was used to image the retina 2 days prior to Glaucoma induction and also 2 days prior to culling. [ABN1] Eyes were collected at D25. The number and location of endogenous Myo/Nog cells were determined by immunofluorescence microscopy. Retinal ganglion cell layer (RGC) and nerve fiber layer (NFL) thickness was further analyzed histologically. Myo/Nog cells isolated from the brain were injected into the anterior chamber to determine their ability to integrate into issues and home to areas of stress. Results : OCT revealed increased optic cup/disk asymmetry and depth, and decreased RGC/NFL thickness after induction of glaucoma. Endogenous Myo/Nog cells were increased around the optic nerve and periphery of the retina compared to normal retinas. Myo/Nog cells injected into the anterior chamber were tracked to areas of stress such as the trabecular meshwork, the ciliary body and the canal of Schlemm. Conclusions : Consistent with our previous studies in other models of retinopathy, Myo/Nog cells increase in number in response to elevated IOP and are concentrated in areas of stress in the retina. Myo/Nog cells injected into the anterior chamber revealed become integrated into tissues that are affected by impaired aqueous humor outflow. The impact of Myo/Nog cells on retinal damage induced by glaucoma is under investigation. This is a 2020 ARVO Annual Meeting abstract.",

author = "Paul Lecker and Karnaveer Johal and John Spikes and Jake Bernstein and McGrath, {Alexa Noel} and Victoria MacPherson and Rushil Brahmbhatt and Mark Martin and Christopher Sutera and Brent Biscoe and Jashanveer Johal and Jacquelyn Gerhart and Grzegorz Gorski and Mindy George-Weinstein and {Bravo Nuevo}, Arturo",

year = "2020",

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doi = "/article.aspx?articleid=2766662",

language = "American English",

note = "ARVO Annual Meeting 2020 ; Conference date: 01-06-2020",

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T1 - Myo/Nog Cells Migrate to Areas of Stress within The Eye in a Mouse Model of Glaucoma

AU - Lecker, Paul

AU - Johal, Karnaveer

AU - Spikes, John

AU - Bernstein, Jake

AU - McGrath, Alexa Noel

AU - MacPherson, Victoria

AU - Brahmbhatt, Rushil

AU - Martin, Mark

AU - Sutera, Christopher

AU - Biscoe, Brent

AU - Johal, Jashanveer

AU - Gerhart, Jacquelyn

AU - Gorski, Grzegorz

AU - George-Weinstein, Mindy

AU - Bravo Nuevo, Arturo

PY - 2020/6

Y1 - 2020/6

N2 - Purpose : Myo/Nog cells were discovered in the early embryo by their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenic protein inhibitor noggin. Their release of noggin is critical for normal embryonic development, including eye morphogenesis. Myo/Nog cells also are present in the adult eye where they respond to stress and injury. Depletion of Myo/Nog cells was associated with increased photoreceptor cell death, while their addition to the vitreous preserved function and reduced cell death following light damage. The goal of this project was to examine the behavior of Myo/Nog cells in response to increased intraocular pressure (IOP) and subsequent retinal damage in a mouse model of glaucoma. Methods : The right eyes of C57BL/6J mice were injected with 2µL of microbeads into the anterior chamber to reduce outflow of aqueous humor and induce a glaucomatous state. IOP was measured prior to bead injection and 4, 7 and 21 days after injection. Optical coherence tomography (OCT) was used to image the retina 2 days prior to Glaucoma induction and also 2 days prior to culling. [ABN1] Eyes were collected at D25. The number and location of endogenous Myo/Nog cells were determined by immunofluorescence microscopy. Retinal ganglion cell layer (RGC) and nerve fiber layer (NFL) thickness was further analyzed histologically. Myo/Nog cells isolated from the brain were injected into the anterior chamber to determine their ability to integrate into issues and home to areas of stress. Results : OCT revealed increased optic cup/disk asymmetry and depth, and decreased RGC/NFL thickness after induction of glaucoma. Endogenous Myo/Nog cells were increased around the optic nerve and periphery of the retina compared to normal retinas. Myo/Nog cells injected into the anterior chamber were tracked to areas of stress such as the trabecular meshwork, the ciliary body and the canal of Schlemm. Conclusions : Consistent with our previous studies in other models of retinopathy, Myo/Nog cells increase in number in response to elevated IOP and are concentrated in areas of stress in the retina. Myo/Nog cells injected into the anterior chamber revealed become integrated into tissues that are affected by impaired aqueous humor outflow. The impact of Myo/Nog cells on retinal damage induced by glaucoma is under investigation. This is a 2020 ARVO Annual Meeting abstract.

AB - Purpose : Myo/Nog cells were discovered in the early embryo by their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenic protein inhibitor noggin. Their release of noggin is critical for normal embryonic development, including eye morphogenesis. Myo/Nog cells also are present in the adult eye where they respond to stress and injury. Depletion of Myo/Nog cells was associated with increased photoreceptor cell death, while their addition to the vitreous preserved function and reduced cell death following light damage. The goal of this project was to examine the behavior of Myo/Nog cells in response to increased intraocular pressure (IOP) and subsequent retinal damage in a mouse model of glaucoma. Methods : The right eyes of C57BL/6J mice were injected with 2µL of microbeads into the anterior chamber to reduce outflow of aqueous humor and induce a glaucomatous state. IOP was measured prior to bead injection and 4, 7 and 21 days after injection. Optical coherence tomography (OCT) was used to image the retina 2 days prior to Glaucoma induction and also 2 days prior to culling. [ABN1] Eyes were collected at D25. The number and location of endogenous Myo/Nog cells were determined by immunofluorescence microscopy. Retinal ganglion cell layer (RGC) and nerve fiber layer (NFL) thickness was further analyzed histologically. Myo/Nog cells isolated from the brain were injected into the anterior chamber to determine their ability to integrate into issues and home to areas of stress. Results : OCT revealed increased optic cup/disk asymmetry and depth, and decreased RGC/NFL thickness after induction of glaucoma. Endogenous Myo/Nog cells were increased around the optic nerve and periphery of the retina compared to normal retinas. Myo/Nog cells injected into the anterior chamber were tracked to areas of stress such as the trabecular meshwork, the ciliary body and the canal of Schlemm. Conclusions : Consistent with our previous studies in other models of retinopathy, Myo/Nog cells increase in number in response to elevated IOP and are concentrated in areas of stress in the retina. Myo/Nog cells injected into the anterior chamber revealed become integrated into tissues that are affected by impaired aqueous humor outflow. The impact of Myo/Nog cells on retinal damage induced by glaucoma is under investigation. This is a 2020 ARVO Annual Meeting abstract.

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