Abstract
Ocular and periocular traumatisms may result in loss of vision. Hypothermia provides a beneficial intervention for brain and heart conditions and, here, we study whether hypothermia can prevent retinal damage caused by traumatic neuropathy. Intraorbital optic nerve crush (IONC) or sham manipulation was applied to male rats. Some animals were subjected to hypothermia (8 °C) for 3 h following surgery. Thirty days later, animals were subjected to electroretinography and behavioral tests. IONC treatment resulted in amplitude reduction of the b-wave and oscillatory potentials of the electroretinogram, whereas the hypothermic treatment significantly (p < 0.05) reversed this process. Using a descending method of limits in a two-choice visual task apparatus, we demonstrated that hypothermia significantly (p < 0.001) preserved visual acuity. Furthermore, IONC-treated rats had a lower (p < 0.0001) number of retinal ganglion cells and a higher (p < 0.0001) number of TUNEL-positive cells than sham-operated controls. These numbers were significantly (p < 0.0001) corrected by hypothermic treatment. There was a significant (p < 0.001) increase of RNA-binding motif protein 3 (RBM3) and of BCL2 (p < 0.01) mRNA expression in the eyes exposed to hypothermia. In conclusion, hypothermia constitutes an efficacious treatment for traumatic vision-impairing conditions, and the cold-shock protein pathway may be involved in mediating the beneficial effects shown in the retina.
Highlights
Among the military population, blasts are the leading cause of disability resulting in traumatic brain and retinal injuries[5]
We have studied the expression of 2 cold-shock proteins (CSP), which increases after exposure to cold temperatures: RNA-binding motif protein 3 (RBM3) and cold inducible RNA-binding protein (CIRP or CIRBP)
In rats kept in normothermia, the eye subjected to intraorbital optic nerve crush (IONC) presented a b-wave with lower amplitude than the sham-operated eye (Fig. 1A)
Summary
Blasts are the leading cause of disability resulting in traumatic brain and retinal injuries[5]. We have studied the expression of 2 cold-shock proteins (CSP), which increases after exposure to cold temperatures: RNA-binding motif protein 3 (RBM3) and cold inducible RNA-binding protein (CIRP or CIRBP) These proteins, which belong to the heterogeneous nuclear ribonucleoprotein family, bind to cellular RNAs and regulate their half-life and their expression potential and their final functions[30,31,32,33,34]. The expression of these proteins in the rat retina has been recently characterized[35] and they may be part of the mechanism by which hypothermia prevents tissue damage. Expression of CSPs and anti-apoptotic signals were upregulated in the animals receiving hypothermic treatment
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