Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa

Abstract Photobiomodulation (PBM) by far-red (FR) to near-infrared (NIR) light has been demonstrated to restore the function of damaged mitochondria, increase the production of cytoprotective factors and prevent cell death. Our laboratory has shown that FR PBM improves functional and structural outc...

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Autores principales:	Sandeep Gopalakrishnan, Shima Mehrvar, Sepideh Maleki, Heather Schmitt, Phyllis Summerfelt, Adam M. Dubis, Betsy Abroe, Thomas B. Connor, Joseph Carroll, Wendy Huddleston, Mahsa Ranji, Janis T. Eells
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2020
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/5aee5cb0967f41f39aadd3c6c79e264a
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spelling	oai:doaj.org-article:5aee5cb0967f41f39aadd3c6c79e264a2021-12-02T12:33:44ZPhotobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa10.1038/s41598-020-77290-w2045-2322https://doaj.org/article/5aee5cb0967f41f39aadd3c6c79e264a2020-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-77290-whttps://doaj.org/toc/2045-2322Abstract Photobiomodulation (PBM) by far-red (FR) to near-infrared (NIR) light has been demonstrated to restore the function of damaged mitochondria, increase the production of cytoprotective factors and prevent cell death. Our laboratory has shown that FR PBM improves functional and structural outcomes in animal models of retinal injury and retinal degenerative disease. The current study tested the hypothesis that a brief course of NIR (830 nm) PBM would preserve mitochondrial metabolic state and attenuate photoreceptor loss in a model of retinitis pigmentosa, the P23H transgenic rat. P23H rat pups were treated with 830 nm light (180 s; 25 mW/cm2; 4.5 J/cm2) using a light-emitting diode array (Quantum Devices, Barneveld, WI) from postnatal day (p) 10 to p25. Sham-treated rats were restrained, but not treated with 830 nm light. Retinal metabolic state, function and morphology were assessed at p30 by measurement of mitochondrial redox (NADH/FAD) state by 3D optical cryo-imaging, electroretinography (ERG), spectral-domain optical coherence tomography (SD-OCT), and histomorphometry. PBM preserved retinal metabolic state, retinal function, and retinal morphology in PBM-treated animals compared to the sham-treated group. PBM protected against the disruption of the oxidation state of the mitochondrial respiratory chain observed in sham-treated animals. Scotopic ERG responses over a range of flash intensities were significantly greater in PBM-treated rats compared to sham controls. SD-OCT studies and histological assessment showed that PBM preserved the structural integrity of the retina. These findings demonstrate for the first time a direct effect of NIR PBM on retinal mitochondrial redox status in a well-established model of retinal disease. They show that chronic proteotoxic stress disrupts retinal bioenergetics resulting in mitochondrial dysfunction, and retinal degeneration and that therapies normalizing mitochondrial metabolism have considerable potential for the treatment of retinal degenerative disease.Sandeep GopalakrishnanShima MehrvarSepideh MalekiHeather SchmittPhyllis SummerfeltAdam M. DubisBetsy AbroeThomas B. ConnorJoseph CarrollWendy HuddlestonMahsa RanjiJanis T. EellsNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 10, Iss 1, Pp 1-13 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sandeep Gopalakrishnan Shima Mehrvar Sepideh Maleki Heather Schmitt Phyllis Summerfelt Adam M. Dubis Betsy Abroe Thomas B. Connor Joseph Carroll Wendy Huddleston Mahsa Ranji Janis T. Eells Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
description	Abstract Photobiomodulation (PBM) by far-red (FR) to near-infrared (NIR) light has been demonstrated to restore the function of damaged mitochondria, increase the production of cytoprotective factors and prevent cell death. Our laboratory has shown that FR PBM improves functional and structural outcomes in animal models of retinal injury and retinal degenerative disease. The current study tested the hypothesis that a brief course of NIR (830 nm) PBM would preserve mitochondrial metabolic state and attenuate photoreceptor loss in a model of retinitis pigmentosa, the P23H transgenic rat. P23H rat pups were treated with 830 nm light (180 s; 25 mW/cm2; 4.5 J/cm2) using a light-emitting diode array (Quantum Devices, Barneveld, WI) from postnatal day (p) 10 to p25. Sham-treated rats were restrained, but not treated with 830 nm light. Retinal metabolic state, function and morphology were assessed at p30 by measurement of mitochondrial redox (NADH/FAD) state by 3D optical cryo-imaging, electroretinography (ERG), spectral-domain optical coherence tomography (SD-OCT), and histomorphometry. PBM preserved retinal metabolic state, retinal function, and retinal morphology in PBM-treated animals compared to the sham-treated group. PBM protected against the disruption of the oxidation state of the mitochondrial respiratory chain observed in sham-treated animals. Scotopic ERG responses over a range of flash intensities were significantly greater in PBM-treated rats compared to sham controls. SD-OCT studies and histological assessment showed that PBM preserved the structural integrity of the retina. These findings demonstrate for the first time a direct effect of NIR PBM on retinal mitochondrial redox status in a well-established model of retinal disease. They show that chronic proteotoxic stress disrupts retinal bioenergetics resulting in mitochondrial dysfunction, and retinal degeneration and that therapies normalizing mitochondrial metabolism have considerable potential for the treatment of retinal degenerative disease.
format	article
author	Sandeep Gopalakrishnan Shima Mehrvar Sepideh Maleki Heather Schmitt Phyllis Summerfelt Adam M. Dubis Betsy Abroe Thomas B. Connor Joseph Carroll Wendy Huddleston Mahsa Ranji Janis T. Eells
author_facet	Sandeep Gopalakrishnan Shima Mehrvar Sepideh Maleki Heather Schmitt Phyllis Summerfelt Adam M. Dubis Betsy Abroe Thomas B. Connor Joseph Carroll Wendy Huddleston Mahsa Ranji Janis T. Eells
author_sort	Sandeep Gopalakrishnan
title	Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
title_short	Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
title_full	Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
title_fullStr	Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
title_full_unstemmed	Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
title_sort	photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa
publisher	Nature Portfolio
publishDate	2020
url	https://doaj.org/article/5aee5cb0967f41f39aadd3c6c79e264a
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Photobiomodulation preserves mitochondrial redox state and is retinoprotective in a rodent model of retinitis pigmentosa

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