β-alanine supplementation induces taurine depletion and causes alterations of the retinal nerve fiber layer and axonal transport by retinal ganglion cells

García‐Ayuso, Diego; Pierdomenico, Johnny Di; Valiente‐Soriano, Francisco J.; Martínez-Vacas, Ana; Agudo‐Barriuso, Marta; Vidal‐Sanz, Manuel; Picaud, Serge; Villegas‐Pérez, María Paz

doi:10.1016/j.exer.2019.107781

Cited by 25 publications

(33 citation statements)

References 49 publications

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“…Similar alterations in the pNFH expression pattern have been observed following other retinal degenerations such as optic nerve transection [71,72], crush [74,76,90], elevation of intraocular pressure [91,92] or taurine depletion [75]. These interesting events, and specifically pNFH expression in the RGC bodies and their dendrites, have been proposed as a feature of RGC degeneration [62], particularly with pathological processes associated with axonal damage and RGC stress [74,75,76].…”

Section: Retinal Remodeling and Retinal Ganglion Cellsmentioning

confidence: 57%

“…So, the question arises: what is the cause of the RGC death during retinal remodeling? We also have extensive experience in the study of the retinal nerve fiber layer (RNFL) by immunodetecting the phosphorylated high-molecular-weight subunit of the neurofilament triplet (pNFH), which in homeostasis is expressed in the intra-retinal RGC axons [71,72,74,75]. Changes in the expression pattern of pNFH is an early hallmark of RGC degeneration, and thus this immunodetection is a very good tool to analyze the course of RGC pathological responses to photoreceptor diseases [9,10,74,76,77].…”

Section: Retinal Remodeling and Retinal Ganglion Cellsmentioning

confidence: 99%

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Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration

García‐Ayuso

Pierdomenico

Vidal‐Sanz

et al. 2019

IJMS

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Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina.

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Section: Retinal Remodeling and Retinal Ganglion Cellsmentioning

confidence: 57%

Section: Retinal Remodeling and Retinal Ganglion Cellsmentioning

confidence: 99%

Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration

García‐Ayuso

Pierdomenico

Vidal‐Sanz

et al. 2019

IJMS

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“…This TauT has a higher affinity for β-amino acids, such as taurine, but a lower affinity for α-amino acids [ 90 ]. The importance of this taurine transporter has been evidenced in mouse models lacking the TauT gene [ 126 , 127 ], as well as in in vivo and in vitro studies utilizing taurine transporter competitive inhibitors, such as β-alanine [ 128 , 129 ] or guanidinoethanesulfonate (GES) [ 130 , 131 ].…”

Section: Taurine Biologymentioning

confidence: 99%

The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant

2021

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Taurine is a naturally occurring sulfur-containing amino acid that is found abundantly in excitatory tissues, such as the heart, brain, retina and skeletal muscles. Taurine was first isolated in the 1800s, but not much was known about this molecule until the 1990s. In 1985, taurine was first approved as the treatment among heart failure patients in Japan. Accumulating studies have shown that taurine supplementation also protects against pathologies associated with mitochondrial defects, such as aging, mitochondrial diseases, metabolic syndrome, cancer, cardiovascular diseases and neurological disorders. In this review, we will provide a general overview on the mitochondria biology and the consequence of mitochondrial defects in pathologies. Then, we will discuss the antioxidant action of taurine, particularly in relation to the maintenance of mitochondria function. We will also describe several reported studies on the current use of taurine supplementation in several mitochondria-associated pathologies in humans.

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“… 1 – 4 Light exposure causes well-documented apoptotic cellular death, mostly to the outer retinal layers. 2 , 5 , 6 Furthermore, light is also a known risk factor for some retinal degenerations 7 , 8 and exacerbates photoreceptor degeneration in some inherited 9 – 12 or induced 13 , 14 retinal degenerations.…”

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confidence: 99%

Coordinated Intervention of Microglial and Müller Cells in Light-Induced Retinal Degeneration

Pierdomenico

Martínez-Vacas

Hernández-Muñoz

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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To analyze the role of microglial and Müller cells in the formation of rings of photoreceptor degeneration caused by phototoxicity. METHODS. Two-month-old Sprague-Dawley rats were exposed to light and processed 1, 2, or 3 months later. Retinas were dissected as whole-mounts, immunodetected for microglial cells, Müller cells, and Sand L/M-cones and analyzed using fluorescence, thunder imaging, and confocal microscopy. Cone populations were automatically counted and isodensity maps constructed to document cone topography. RESULTS. Phototoxicity causes a significant progressive loss of Sand L/M-cones of up to 68% and 44%, respectively, at 3 months after light exposure (ALE). One month ALE, we observed rings of cone degeneration in the photosensitive area of the superior retina. Two and 3 months ALE, these rings had extended to the central and inferior retina. Within the rings of cone degeneration, there were degenerating cones, often activated microglial cells, and numerous radially oriented processes of Müller cells that showed increased expression of intermediate filaments. Between 1 and 3 months ALE, the rings coalesced, and at the same time the microglial cells resumed a mosaic-like distribution, and there was a decrease of Müller cell gliosis at the areas devoid of cones. CONCLUSIONS. Light-induced photoreceptor degeneration proceeds with rings of cone degeneration, as observed in inherited retinal degenerations in which cone death is secondary to rod degeneration. The spatiotemporal relationship of cone death microglial cell activation and Müller cell gliosis within the rings of cone degeneration suggests that, although both glial cells are involved in the formation of the rings, they may have coordinated actions and, while microglial cells may be more involved in photoreceptor phagocytosis, Müller cells may be more involved in cone and microglial cell migration, retinal remodeling and glial seal formation.

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β-alanine supplementation induces taurine depletion and causes alterations of the retinal nerve fiber layer and axonal transport by retinal ganglion cells

Cited by 25 publications

References 49 publications

Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration

Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration

The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant

Coordinated Intervention of Microglial and Müller Cells in Light-Induced Retinal Degeneration

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