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Thioredoxin 1 Plays a Protective Role in Retinas Exposed to Perinatal Hypoxia-Ischemia
M I Holubiec1, P Galeano2, J I Romero2
1Laboratorio de Citoarquitectura y Plasticidad Neuronal, Instituto de Investigaciones Cardiológicas "Prof. Dr. Alberto C. Taquini" (ININCA), Facultad de Medicina (UBA-CONICET), Buenos Aires, Argentina; Instituto de Investigaciones Bioquímicas de Buenos Aires (IIBBA-CONICET), Argentina.
Insights
Thioredoxin 1 (Trx1) plays a crucial role in protecting the retina from perinatal hypoxia-ischemia (PHI) damage. Restoring Trx1 levels in PHI-affected animals improved neurodevelopment and reduced retinal injury.
Area of Science:
- Biochemistry
- Neuroscience
- Ophthalmology
Background:
- Thioredoxin family proteins regulate cellular redox balance.
- Perinatal hypoxia-ischemia (PHI) severely impacts the developing central nervous system, particularly the retina.
- PHI can lead to retinopathy of prematurity, causing vision impairment and blindness.
Purpose of the Study:
- To investigate the role of thioredoxin 1 (Trx1) in retinal damage following PHI.
- To evaluate Trx1 as a potential therapeutic target for PHI-induced retinopathy.
Main Methods:
- Utilized in vivo rat models of PHI (perinatal asphyxia, carotid ligation).
- Employed the ARPE-19 cell line exposed to hypoxia and reoxygenation.
- Analyzed Trx1 protein levels, performed Trx1 knock-down, and administered recombinant Trx1.
Main Results:
- Observed significant alterations in Trx1 protein levels in both animal and cell models post-PHI.
- Trx1 knock-down in ARPE-19 cells impacted cell morphology, proliferation, and differentiation markers.
- Recombinant Trx1 administration reduced astrogliosis and ameliorated delayed neurodevelopment in PHI rats.
Conclusions:
- Trx1 is significantly affected by PHI in the retina.
- Trx1 modulation influences retinal cell behavior and neurodevelopment.
- Trx1 represents a promising therapeutic agent for mitigating birth-related retinal injury.
Abstract:
Thioredoxin family proteins are key modulators of cellular redox regulation and have been linked to several physiological functions, including the cellular response to hypoxia-ischemia. During perinatal hypoxia-ischemia (PHI), the central nervous system is subjected to a fast decrease in O2 and nutrients with a subsequent reoxygenation that ultimately leads to the production of reactive species impairing physiological redox signaling. Particularly, the retina is one of the most affected tissues, due to its high oxygen consumption and exposure to light. One of the main consequences of PHI is retinopathy of prematurity, comprising changes in retinal neural and vascular development, with further compensatory mechanisms that can ultimately lead to retinal detachment and blindness. In this study, we have analyzed long-term changes that occur in the retina using two well established in vivo rat PHI models (perinatal asphyxia and carotid ligation model), as well as the ARPE-19 cell line that was exposed to hypoxia and reoxygenation. We observed significant changes in the protein levels of the cytosolic oxidoreductase thioredoxin 1 (Trx1) in both animal models and a cell model. Knock-down of Trx1 in ARPE-19 cells affected cell morphology, proliferation and the levels of specific differentiation markers. Administration of recombinant Trx1 decreased astrogliosis and improved delayed neurodevelopment in animals exposed to PHI. Taken together, our results suggest therapeutical implications for Trx1 in retinal damage induced by hypoxia-ischemia during birth.
