Lactate-Mediated Protection of Retinal Ganglion Cells

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Lactate-Mediated Protection of Retinal Ganglion Cells. / Vohra, Rupali; Aldana, Blanca I.; Bulli, Giorgia; Skytt, Dorte M.; Waagepetersen, Helle; Bergersen, Linda H.; Kolko, Miriam.

In: Journal of Molecular Biology, Vol. 431, No. 9, 19.04.2019, p. 1878-1888.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vohra, R, Aldana, BI, Bulli, G, Skytt, DM, Waagepetersen, H, Bergersen, LH & Kolko, M 2019, 'Lactate-Mediated Protection of Retinal Ganglion Cells', Journal of Molecular Biology, vol. 431, no. 9, pp. 1878-1888. https://doi.org/10.1016/j.jmb.2019.03.005

APA

Vohra, R., Aldana, B. I., Bulli, G., Skytt, D. M., Waagepetersen, H., Bergersen, L. H., & Kolko, M. (2019). Lactate-Mediated Protection of Retinal Ganglion Cells. Journal of Molecular Biology, 431(9), 1878-1888. https://doi.org/10.1016/j.jmb.2019.03.005

Vancouver

Vohra R, Aldana BI, Bulli G, Skytt DM, Waagepetersen H, Bergersen LH et al. Lactate-Mediated Protection of Retinal Ganglion Cells. Journal of Molecular Biology. 2019 Apr 19;431(9):1878-1888. https://doi.org/10.1016/j.jmb.2019.03.005

Author

Vohra, Rupali ; Aldana, Blanca I. ; Bulli, Giorgia ; Skytt, Dorte M. ; Waagepetersen, Helle ; Bergersen, Linda H. ; Kolko, Miriam. / Lactate-Mediated Protection of Retinal Ganglion Cells. In: Journal of Molecular Biology. 2019 ; Vol. 431, No. 9. pp. 1878-1888.

Bibtex

@article{551f27f76d3c4e3a823d62b168326150,
title = "Lactate-Mediated Protection of Retinal Ganglion Cells",
abstract = "Loss of retinal ganglion cells (RGCs) is a leading cause of blinding conditions. The purpose of this study was to evaluate the effect of extracellular L-lactate on RGC survival facilitated through lactate metabolism and ATP production. We identified lactate as a preferred energy substrate over glucose in murine RGCs and showed that lactate metabolism and consequently increased ATP production are crucial components in promoting RGC survival during energetic crisis. Lactate was released to the extracellular environment in the presence of glucose and detained intracellularly during glucose deprivation. Lactate uptake and metabolism was unaltered in the presence and absence of glucose. However, the ATP production declined significantly for 24 h of glucose deprivation and increased significantly in the presence of lactate. Finally, lactate exposure for 2 and 24 h resulted in increased RGC survival during glucose deprivation. In conclusion, the metabolic pathway of lactate in RGCs may be of great future interest to unravel potential pharmaceutical targets, ultimately leading to novel therapies in the prevention of blinding neurodegenerative diseases, for example, glaucoma.",
keywords = "energy metabolism, lactate, M{\"u}ller cells, retinal ganglion cells",
author = "Rupali Vohra and Aldana, {Blanca I.} and Giorgia Bulli and Skytt, {Dorte M.} and Helle Waagepetersen and Bergersen, {Linda H.} and Miriam Kolko",
year = "2019",
month = "4",
day = "19",
doi = "10.1016/j.jmb.2019.03.005",
language = "English",
volume = "431",
pages = "1878--1888",
journal = "Journal of Molecular Biology",
issn = "0022-2836",
publisher = "Academic Press",
number = "9",

}

RIS

TY - JOUR

T1 - Lactate-Mediated Protection of Retinal Ganglion Cells

AU - Vohra, Rupali

AU - Aldana, Blanca I.

AU - Bulli, Giorgia

AU - Skytt, Dorte M.

AU - Waagepetersen, Helle

AU - Bergersen, Linda H.

AU - Kolko, Miriam

PY - 2019/4/19

Y1 - 2019/4/19

N2 - Loss of retinal ganglion cells (RGCs) is a leading cause of blinding conditions. The purpose of this study was to evaluate the effect of extracellular L-lactate on RGC survival facilitated through lactate metabolism and ATP production. We identified lactate as a preferred energy substrate over glucose in murine RGCs and showed that lactate metabolism and consequently increased ATP production are crucial components in promoting RGC survival during energetic crisis. Lactate was released to the extracellular environment in the presence of glucose and detained intracellularly during glucose deprivation. Lactate uptake and metabolism was unaltered in the presence and absence of glucose. However, the ATP production declined significantly for 24 h of glucose deprivation and increased significantly in the presence of lactate. Finally, lactate exposure for 2 and 24 h resulted in increased RGC survival during glucose deprivation. In conclusion, the metabolic pathway of lactate in RGCs may be of great future interest to unravel potential pharmaceutical targets, ultimately leading to novel therapies in the prevention of blinding neurodegenerative diseases, for example, glaucoma.

AB - Loss of retinal ganglion cells (RGCs) is a leading cause of blinding conditions. The purpose of this study was to evaluate the effect of extracellular L-lactate on RGC survival facilitated through lactate metabolism and ATP production. We identified lactate as a preferred energy substrate over glucose in murine RGCs and showed that lactate metabolism and consequently increased ATP production are crucial components in promoting RGC survival during energetic crisis. Lactate was released to the extracellular environment in the presence of glucose and detained intracellularly during glucose deprivation. Lactate uptake and metabolism was unaltered in the presence and absence of glucose. However, the ATP production declined significantly for 24 h of glucose deprivation and increased significantly in the presence of lactate. Finally, lactate exposure for 2 and 24 h resulted in increased RGC survival during glucose deprivation. In conclusion, the metabolic pathway of lactate in RGCs may be of great future interest to unravel potential pharmaceutical targets, ultimately leading to novel therapies in the prevention of blinding neurodegenerative diseases, for example, glaucoma.

KW - energy metabolism

KW - lactate

KW - Müller cells

KW - retinal ganglion cells

U2 - 10.1016/j.jmb.2019.03.005

DO - 10.1016/j.jmb.2019.03.005

M3 - Journal article

VL - 431

SP - 1878

EP - 1888

JO - Journal of Molecular Biology

JF - Journal of Molecular Biology

SN - 0022-2836

IS - 9

ER -

ID: 216915737