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Adrianna Latuszek, Rajeevalochan Wudali, Ying Hu, Carmelo Romano; Retinal physiological changes in Thyroid Stimulating Hormone Receptor Knock Out mice. Invest. Ophthalmol. Vis. Sci. 2019;60(9):3116. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
The typical mammalian visual system has two photoreceptor types: rods for dim light vision, cones for color vision. Transcription factors such as thyroid hormone (Th) play critical role in photoreceptor differentiation. For example, Thrb2-/- mice lack M cones, instead all cones express S opsin. Thyroid Stimulating Hormone Receptor (Tshr) knockout (KO) mice have been used as a model of congenital hypothyroidism. However, Tshr expression and physiological consequences of Tshr KO eye haven’t been studied. In the present study, we investigated the Tshr expression pattern, morphological and physiological changes in eyes of adult Tshr KO mice.
Adult Velocigene Tshr-/-, Tshr-+/+ and age matched C57BL/6J mice were assessed using optical coherence tomography (OCT) and electroretinography (ERG). Retinal pigment epithelial (RPE) cell function was assessed using a “C” Wave protocol, photoreceptor function was assessed using scotopic protocol, photopic and flicker ERG protocols.
In all ERG protocols we tested, the responses from Tshr KO mice showed significantly decreased ERG amplitudes compared to WT and aged matched C57BL/6J mice. However, no significant retinal morphological changes were observed in Tshr KO mice by OCT. In house NGS data in African Green Monkey (AGM) shows that Tshr is highly expressed in the RPE compared to the other parts of the eye.
Deleting Tshr gene causes long term physiological deficit in the rods, cones and RPE cells. Since RPE plays an important role in photoreceptor hemostasis and function, Tsh might play important role in photoreceptor differentiation not only through direct effect of T3, T4 on Th receptors but also indirectly through the RPE cells.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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