Neuroprotection from optic nerve injury and modulation of oxidative metabolism by transplantation of active mitochondria to the retina

Publication date: Available online 15 January 2020Source: Biochimica et Biophysica Acta (BBA) - Molecular Basis of DiseaseAuthor(s): Gabriel Nascimento-dos-Santos, Eduardo de-Souza-Ferreira, Rafael Lani, Caroline Coelho de Faria, Victor Guedes Araujo, Leandro Coelho Teixeira-Pinheiro, Taliane de Souza Vasconcelos, Thaís Gonçalo Leandro, Marcelo Felippe Santiago, Rafael Linden, Antonio Galina, Hilda Petrs-SilvaAbstractMitochondrial dysfunctions are linked to a series of neurodegenerative human conditions, including Parkinson's disease, schizophrenia, optic neuropathies, and glaucoma. Recently, a series of studies have pointed mitotherapy – exogenous mitochondria transplant – as a promising way to attenuate the progression of neurologic disorders; however, the neuroprotective and pro-regenerative potentials of isolated mitochondria in vivo have not yet been elucidated. In this present work, we tested the effects of transplants of active (as well-coupled organelles were named), liver-isolated mitochondria on the survival of retinal ganglion cells and axonal outgrowth after optic nerve crush. Our data show that intravitreally transplanted, full active mitochondria incorporate into the retina, improve its oxidative metabolism and electrophysiological activity at 1 day after transplantation. Moreover, mitotherapy increases cell survival in the ganglion cell layer at 14 days, and leads to a higher number of axons extending beyond the injury site at 28 days; effects that ...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research