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Article ; Online: Contralateral Astrocyte Response to Acute Optic Nerve Damage Is Mitigated by PANX1 Channel Activity.

Wurl, Jasmine A / Mac Nair, Caitlin E / Dietz, Joel A / Shestopalov, Valery I / Nickells, Robert W

International journal of molecular sciences

2023 Volume 24, Issue 21

Abstract: Glial reactivity is considered a hallmark of damage-induced innate immune responses in the central nervous system. In the visual system, unilateral optic nerve damage elicits dramatic glial reactivity in the retina directly affected by the lesion and a ... ...

Abstract	Glial reactivity is considered a hallmark of damage-induced innate immune responses in the central nervous system. In the visual system, unilateral optic nerve damage elicits dramatic glial reactivity in the retina directly affected by the lesion and a similar, albeit more modest, effect in the contralateral eye. Evaluation of astrocyte changes in a mouse model of optic nerve crush indicates that astrocyte reactivity, as a function of retinal coverage and cellular hypertrophy, occurs within both the experimental and contralateral retinas, although the hypertrophic response of the astrocytes in the contralateral eyes is delayed for at least 24 h. Evaluation of astrocytic reactivity as a function of
MeSH term(s)	Mice ; Animals ; Astrocytes/metabolism ; Neuroglia/metabolism ; Retina/metabolism ; Optic Nerve Injuries/metabolism ; Optic Nerve/pathology ; Glial Fibrillary Acidic Protein/metabolism ; Nerve Tissue Proteins/metabolism ; Connexins/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein ; Panx1 protein, mouse ; Nerve Tissue Proteins ; Connexins
Language	English
Publishing date	2023-10-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242115641
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Article ; Online: The Long-Term Effects on the Retina Damaged by Optic Nerve Axotomy.

Nickells, Robert W

Investigative ophthalmology & visual science

2015 Volume 56, Issue 10, Page(s) 6113

MeSH term(s)	Animals ; Axotomy/adverse effects ; Optic Nerve/pathology ; Optic Nerve Injuries/complications ; Retinal Diseases/pathology ; Retinal Ganglion Cells/pathology ; gamma-Synuclein/biosynthesis
Chemical Substances	gamma-Synuclein
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.15-17997
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Article ; Online: Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis.

Grosser, Joshua A / Maes, Margaret E / Nickells, Robert W

Apoptosis : an international journal on programmed cell death

2021 Volume 26, Issue 1-2, Page(s) 132–145

Abstract: Recent advancements in live cell imaging technologies have identified the phenomenon of intracellular propagation of late apoptotic events, such as cytochrome c release and caspase activation. The mechanism, prevalence, and speed of apoptosis propagation ...

Abstract	Recent advancements in live cell imaging technologies have identified the phenomenon of intracellular propagation of late apoptotic events, such as cytochrome c release and caspase activation. The mechanism, prevalence, and speed of apoptosis propagation remain unclear. Additionally, no studies have demonstrated propagation of the pro-apoptotic protein, BAX. To evaluate the role of BAX in intracellular apoptotic propagation, we used high speed live-cell imaging to visualize fluorescently tagged-BAX recruitment to mitochondria in four immortalized cell lines. We show that propagation of mitochondrial BAX recruitment occurs in parallel to cytochrome c and SMAC/Diablo release and is affected by cellular morphology, such that cells with processes are more likely to exhibit propagation. The initiation of propagation events is most prevalent in the distal tips of processes, while the rate of propagation is influenced by the 2-dimensional width of the process. Propagation was rarely observed in the cell soma, which exhibited near synchronous recruitment of BAX. Propagation velocity is not affected by mitochondrial volume in segments of processes, but is negatively affected by mitochondrial density. There was no evidence of a propagating wave of increased levels of intracellular calcium ions. Alternatively, we did observe a uniform increase in superoxide build-up in cellular mitochondria, which was released as a propagating wave simultaneously with the propagating recruitment of BAX to the mitochondrial outer membrane.
MeSH term(s)	Apoptosis ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Cytochromes c/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Superoxides/metabolism ; bcl-2-Associated X Protein/genetics ; bcl-2-Associated X Protein/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; DIABLO protein, human ; Mitochondrial Proteins ; bcl-2-Associated X Protein ; Superoxides (11062-77-4) ; Cytochromes c (9007-43-6)
Language	English
Publishing date	2021-01-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1452360-7
ISSN	1573-675X ; 1360-8185
ISSN (online)	1573-675X
ISSN	1360-8185
DOI	10.1007/s10495-020-01654-w
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Article: BclX

Marola, Olivia J / Yablonski, Sarah E R / Shrager, Peter G / Nickells, Robert W / Libby, Richard T

Cell death discovery

2022 Volume 8, Issue 1, Page(s) 331

Language	English
Publishing date	2022-07-22
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-022-01111-4
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Article ; Online: BCLX

Donahue, Ryan J / Fehrman, Rachel L / Gustafson, Jenna R / Nickells, Robert W

Cell death & disease

2021 Volume 12, Issue 8, Page(s) 781

Abstract: Axonal degeneration of retinal ganglion cells (RGCs) causes blindness in glaucoma. Currently, there are no therapies that target axons to prevent them from degenerating. Activation of the BAX protein has been shown to be the determining step in the ... ...

Abstract	Axonal degeneration of retinal ganglion cells (RGCs) causes blindness in glaucoma. Currently, there are no therapies that target axons to prevent them from degenerating. Activation of the BAX protein has been shown to be the determining step in the intrinsic apoptotic pathway that causes RGCs to die in glaucoma. A putative role for BAX in axonal degeneration is less well elucidated. BCLX
MeSH term(s)	Aging/pathology ; Animals ; Dependovirus ; Disease Models, Animal ; Genetic Therapy ; Glaucoma/complications ; Glaucoma/physiopathology ; Glaucoma/therapy ; Green Fluorescent Proteins/metabolism ; Intraocular Pressure ; Mice, Inbred DBA ; Mitochondria/metabolism ; Nerve Crush ; Nerve Degeneration/complications ; Nerve Degeneration/pathology ; Neurons/pathology ; Optic Nerve/metabolism ; Optic Nerve/pathology ; Protein Transport ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Retinal Ganglion Cells/metabolism ; bcl-X Protein/genetics ; bcl-X Protein/therapeutic use ; Mice
Chemical Substances	RNA, Messenger ; bcl-X Protein ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2021-08-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-021-04068-x
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Article ; Online: BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.

Maes, Margaret E / Donahue, Ryan J / Schlamp, Cassandra L / Marola, Olivia J / Libby, Richard T / Nickells, Robert W

Molecular neurodegeneration

2023 Volume 18, Issue 1, Page(s) 67

Abstract: Background: Pro-apoptotic BAX is a central mediator of retinal ganglion cell (RGC) death after optic nerve damage. BAX activation occurs in two stages including translocation of latent BAX to the mitochondrial outer membrane (MOM) and then ... ...

Abstract	Background: Pro-apoptotic BAX is a central mediator of retinal ganglion cell (RGC) death after optic nerve damage. BAX activation occurs in two stages including translocation of latent BAX to the mitochondrial outer membrane (MOM) and then permeabilization of the MOM to facilitate the release of apoptotic signaling molecules. As a critical component of RGC death, BAX is an attractive target for neuroprotective therapies and an understanding of the kinetics of BAX activation and the mechanisms controlling the two stages of this process in RGCs is potentially valuable in informing the development of a neuroprotective strategy. Methods: The kinetics of BAX translocation were assessed by both static and live-cell imaging of a GFP-BAX fusion protein introduced into RGCs using AAV2-mediated gene transfer in mice. Activation of BAX was achieved using an acute optic nerve crush (ONC) protocol. Live-cell imaging of GFP-BAX was achieved using explants of mouse retina harvested 7 days after ONC. Kinetics of translocation in RGCs were compared to GFP-BAX translocation in 661W tissue culture cells. Permeabilization of GFP-BAX was assessed by staining with the 6A7 monoclonal antibody, which recognizes a conformational change in this protein after MOM insertion. Assessment of individual kinases associated with both stages of activation was made using small molecule inhibitors injected into the vitreous either independently or in concert with ONC surgery. The contribution of the Dual Leucine Zipper-JUN-N-Terminal Kinase cascade was evaluated using mice with a double conditional knock-out of both Mkk4 and Mkk7. Results: ONC induces the translocation of GFP-BAX in RGCs at a slower rate and with less intracellular synchronicity than 661W cells, but exhibits less variability among mitochondrial foci within a single cell. GFP-BAX was also found to translocate in all compartments of an RGC including the dendritic arbor and axon. Approximately 6% of translocating RGCs exhibited retrotranslocation of BAX immediately following translocation. Unlike tissue culture cells, which exhibit simultaneous translocation and permeabilization, RGCs exhibited a significant delay between these two stages, similar to detached cells undergoing anoikis. Translocation, with minimal permeabilization could be induced in a subset of RGCs using an inhibitor of Focal Adhesion Kinase (PF573228). Permeabilization after ONC, in a majority of RGCs, could be inhibited with a broad spectrum kinase inhibitor (sunitinib) or a selective inhibitor for p38/MAPK14 (SB203580). Intervention of DLK-JNK axis signaling abrogated GFP-BAX translocation after ONC. Conclusions: A comparison between BAX activation kinetics in tissue culture cells and in cells of a complex tissue environment shows distinct differences indicating that caution should be used when translating findings from one condition to the other. RGCs exhibit both a delay between translocation and permeabilization and the ability for translocated BAX to be retrotranslocated, suggesting several stages at which intervention of the activation process could be exploited in the design of a therapeutic strategy.
MeSH term(s)	Animals ; Mice ; Retinal Ganglion Cells ; bcl-2-Associated X Protein ; Optic Nerve ; Antibodies, Monoclonal ; Apoptosis
Chemical Substances	bcl-2-Associated X Protein ; Antibodies, Monoclonal
Language	English
Publishing date	2023-09-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-023-00659-8
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Article ; Online: The cell and molecular biology of glaucoma: mechanisms of retinal ganglion cell death.

Nickells, Robert W

Investigative ophthalmology & visual science

2012 Volume 53, Issue 5, Page(s) 2476–2481

MeSH term(s)	Animals ; Apoptosis/physiology ; Apoptosis Regulatory Proteins/physiology ; Axons/physiology ; Genes, bcl-2/physiology ; Glaucoma/genetics ; Glaucoma/metabolism ; Glaucoma/physiopathology ; Humans ; Mice ; Nerve Degeneration/physiopathology ; Proto-Oncogene Proteins c-bcl-2/physiology ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/physiology ; bcl-2-Associated X Protein/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; Proto-Oncogene Proteins c-bcl-2 ; bcl-2-Associated X Protein
Language	English
Publishing date	2012-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.12-9483h
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Article ; Online: Targeting HDAC3 in the DBA/2J spontaneous mouse model of glaucoma.

Schmitt, Heather M / Grosser, Joshua A / Schlamp, Cassandra L / Nickells, Robert W

Experimental eye research

2020 Volume 200, Page(s) 108244

Abstract: High intraocular pressure (IOP) is the most common risk factor associated with glaucoma in humans. While lowering IOP is effective at reducing the rate of retinal ganglion cell (RGC) loss, to date, no treatment exists to directly preserve these cells ... ...

Abstract	High intraocular pressure (IOP) is the most common risk factor associated with glaucoma in humans. While lowering IOP is effective at reducing the rate of retinal ganglion cell (RGC) loss, to date, no treatment exists to directly preserve these cells affected by damage to the optic nerve. Recently, histone deacetylase-3 (HDAC3) has become a potential therapeutic target because it plays an important role in the early nuclear atrophic events that precede RGC death. Conditional knockout or inhibition of HDAC3 prevents histone deacetylation, heterochromatin formation, apoptosis, and eventual RGC loss following acute optic nerve injury. Using these approaches to repress HDAC3 activity, we tested whether targeting HDAC3 protects RGCs from ganglion cell-specific BRN3A expression loss, total somatic cell loss, and optic nerve degeneration in the DBA/2J mouse model of spontaneous glaucoma. Targeted ablation of Hdac3 activity did not protect RGCs from axonal degeneration or somatic cell death in the DBA/2J mouse model of glaucoma. However, inhibition of HDAC3 activity using RGFP966 conferred mild protection against somatic cell loss in the ganglion cell layer in aged DBA/2J mice. Further experimentation is necessary to determine whether other class I HDACs may serve as potential therapeutic targets in chronic models of glaucoma.
MeSH term(s)	Animals ; Disease Models, Animal ; Gene Expression Regulation ; Glaucoma/diagnosis ; Glaucoma/genetics ; Glaucoma/metabolism ; Histone Deacetylases/biosynthesis ; Histone Deacetylases/genetics ; Intraocular Pressure/physiology ; Mice ; Mice, Inbred DBA ; Optic Nerve/metabolism ; Optic Nerve/pathology ; Optic Nerve/physiopathology ; RNA/genetics ; Retinal Ganglion Cells/metabolism ; Retinal Ganglion Cells/pathology
Chemical Substances	RNA (63231-63-0) ; Histone Deacetylases (EC 3.5.1.98) ; histone deacetylase 3 (EC 3.5.1.98)
Language	English
Publishing date	2020-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2020.108244
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Article ; Online: WITHDRAWN: Reprint of: Variations in the rheostat model of apoptosis: What studies of retinal ganglion cell death tell us about the functions of the Bcl2 family proteins.

Nickells, Robert W

Experimental eye research

2011

Abstract: The Publisher regrets that this article is an accidental duplication of an article that has already been published, doi:10.1016/j.exer.2010.03.004. The duplicate article has therefore been withdrawn. ...

Abstract	The Publisher regrets that this article is an accidental duplication of an article that has already been published, doi:10.1016/j.exer.2010.03.004. The duplicate article has therefore been withdrawn.
Language	English
Publishing date	2011-07-29
Publishing country	England
Document type	Journal Article
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2011.07.013
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Article ; Online: The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis.

Grosser, Joshua A / Fehrman, Rachel L / Keefe, Dennis / Redmon, Martin / Nickells, Robert W

BMC research notes

2021 Volume 14, Issue 1, Page(s) 198

Abstract: Objective: Elamipretide (SS31) is a mitochondria-targeted peptide that has reported functions of stabilizing mitochondrial cristae structure and improving mitochondrial bioenergetics. Several studies have documented cell protective features of this ... ...

Abstract	Objective: Elamipretide (SS31) is a mitochondria-targeted peptide that has reported functions of stabilizing mitochondrial cristae structure and improving mitochondrial bioenergetics. Several studies have documented cell protective features of this peptide, including impairment of intrinsic apoptosis by inhibiting the recruitment and activation of the pro-apoptotic BAX protein. We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively. Result: In nucleofected and plated ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria. In the presence of the apoptotic stimulator, staurosporine, cells treated with elamipretide exhibited moderately slower rates of BAX recruitment. Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited. Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death. These results indicate that the protective effect of elamipretide is not at the level of BAX activity to induce pro-apoptotic mitochondrial dysfunction after the initiation of staurosporine-induced apoptosis.
MeSH term(s)	Apoptosis ; Mitochondria ; Oligopeptides/pharmacology ; bcl-2-Associated X Protein
Chemical Substances	Oligopeptides ; arginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamide ; bcl-2-Associated X Protein
Language	English
Publishing date	2021-05-22
Publishing country	England
Document type	Journal Article
ZDB-ID	2413336-X
ISSN	1756-0500 ; 1756-0500
ISSN (online)	1756-0500
ISSN	1756-0500
DOI	10.1186/s13104-021-05613-9
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