The expression of syntaphilin is down-regulated in the optic nerve after axonal injury

Miki, Akiko; Kanamori, Akira; Nakamura, Makoto; Matsumoto, Yoshiko; Mizokami, Junji; Negi, Akira

doi:10.1016/j.exer.2014.10.017

Cited by 3 publications

(2 citation statements)

References 32 publications

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“…Another group of mitochondria remains anchored to the microtubules via syntaphilin, a mitochondrial outer membrane-attached protein, and an actin cytoskeleton component ( Pathak et al, 2010 ). Interestingly, syntaphilin is only expressed in the soma and not in the axon of rat RGCs, suggesting that axons regulate their stationary pool of mitochondria differently from other neurons ( Miki et al, 2014 ). Mitochondrial trafficking can be visualized via video microscopy using a fluorescent dye such as tetramethylrhodamine or fluorescent protein-labeled mitochondria.…”

Section: Mitochondria Of Rgcs: Critical Target Of Metal Ionsmentioning

confidence: 99%

Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury

Tang

Zhuo

2021

Front. Cell Dev. Biol.

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Glaucoma is the most substantial cause of irreversible blinding, which is accompanied by progressive retinal ganglion cell damage. Retinal ganglion cells are energy-intensive neurons that connect the brain and retina, and depend on mitochondrial homeostasis to transduce visual information through the brain. As cofactors that regulate many metabolic signals, iron and zinc have attracted increasing attention in studies on neurons and neurodegenerative diseases. Here, we summarize the research connecting iron, zinc, neuronal mitochondria, and glaucomatous injury, with the aim of updating and expanding the current view of how retinal ganglion cells degenerate in glaucoma, which can reveal novel potential targets for neuroprotection.

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Section: Mitochondria Of Rgcs: Critical Target Of Metal Ionsmentioning

confidence: 99%

Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury

Tang

Zhuo

2021

Front. Cell Dev. Biol.

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“…Therefore, it is difficult to speculate on whether the high density of mitochondria in large axons of the GL region is regulated by a specific machinery of mitochondrial proteins such as the axonal specific and canonical mitochondrial anchoring protein syntaphilin (SNPH) (Kang et al, 2008 ). Interestingly, no expression of SNPH was detected in rat optic nerve axons (Miki et al, 2014 ) suggesting that RGC axons regulate their stationary pool of mitochondria differently than other neurons of the central nervous system such as cortical neurons (Kang et al, 2008 ). Proteomic profiling of mitochondria from axons of the GL could help understand how RGC axons anchor their mitochondria in this region.…”

Section: Discussionmentioning

confidence: 99%

Local Accumulation of Axonal Mitochondria in the Optic Nerve Glial Lamina Precedes Myelination

et al. 2021

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Mitochondria are essential for neurons and must be optimally distributed along their axon to fulfill local functions. A high density of mitochondria has been observed in retinal ganglion cell (RGC) axons of an unmyelinated region of the optic nerve, called the glial lamina (GL) in mouse (lamina cribrosa in human). In glaucoma, the world's leading cause of irreversible blindness, the GL is the epicenter of RGC degeneration and is connected to mitochondrial dysfunction. It is generally accepted that the local accumulation of mitochondria in the GL is established due to the higher energy requirement of unmyelinated axons. Here we revisit the connection between mitochondrial positioning and myelin in RGC axons. We show that the high density of mitochondria in the GL is restricted to larger axons and is established before myelination. Thus, contrary to a longstanding belief in the field, the myelination pattern is not responsible for the establishment of the local accumulation of mitochondria in GL axons. Our findings open new research avenues likely critical to understanding the pathophysiology of glaucoma.

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Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury

Zhang

Botchway

et al. 2023

Mol Neurobiol

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The expression of syntaphilin is down-regulated in the optic nerve after axonal injury

Cited by 3 publications

References 32 publications

Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury

Effects of Iron and Zinc on Mitochondria: Potential Mechanisms of Glaucomatous Injury

Local Accumulation of Axonal Mitochondria in the Optic Nerve Glial Lamina Precedes Myelination

Syntaphilin Inactivation Can Enhance Axonal Mitochondrial Transport to Improve Spinal Cord Injury

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