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dc.contributor.authorHolubiec M.I.
dc.contributor.authorGaleano P.
dc.contributor.authorRomero J.I.
dc.contributor.authorHanschmann E.-M.
dc.contributor.authorLillig C.H.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:20:31Z
dc.date.available2020-09-02T22:20:31Z
dc.date.issued2020
dc.identifier10.1016/j.neuroscience.2019.11.011
dc.identifier.citation425, , 235-250
dc.identifier.issn03064522
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4905
dc.descriptionThioredoxin 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. © 2019 IBRO
dc.language.isoen
dc.publisherElsevier Ltd
dc.subjectperinatal hypoxia–ischemia
dc.subjectreoxygenation
dc.subjectretina
dc.subjectRPE cells
dc.subjectthioredoxin 1
dc.subjectcell marker
dc.subjectgreen fluorescent protein
dc.subjectneurogenic differentiation factor
dc.subjectrecombinant protein
dc.subjectthioredoxin 1
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectARPE-19 cell line
dc.subjectArticle
dc.subjectastrocytosis
dc.subjectcarotid artery ligation
dc.subjectcell differentiation
dc.subjectcell proliferation
dc.subjectcell structure
dc.subjectcontrolled study
dc.subjectfemale
dc.subjectin vivo study
dc.subjectischemia
dc.subjectnonhuman
dc.subjectperinatal asphyxia
dc.subjectperinatal hypoxia ischemia
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectrat
dc.subjectreoxygenation
dc.subjectretina
dc.titleThioredoxin 1 Plays a Protective Role in Retinas Exposed to Perinatal Hypoxia–Ischemia
dc.typeArticle


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