Related Experiment Video
Updated: May 4, 2026

A Novel Light Damage Paradigm for Use in Retinal Regeneration Studies in Adult Zebrafish
Published on: October 24, 2013
Spatiotemporal changes in NFATc4 expression of retinal ganglion cells after light-induced damage
1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, Guangdong Province, People's Republic of China.
Abstract:
Nuclear factor of activated T cells, cytoplasmic 4 (NFATc4) is one of the four members of the NFAT family, which were described first as essential components of T cells activation and lately as important regulators for the initiation and coordination of the immune response, including B cells and natural killer cells. Accumulating evidence has demonstrated that NFATc4 exerted a pro-apoptotic effect in the pathogenesis of various experimental central nervous system diseases by upregulating Fas ligand (FasL) levels. However, the function of NFATc4 in the retina is still with limited acquaintance. To investigate whether NFATc4 is involved in retinal neuron apoptosis, we performed a light-induced retinal damage model in adult rats. A significant upregulation of NFATc4 was detected in the retina after light-induced damage by using Western blotting and reverse transcriptase PCR (RT-PCR). Besides this, NFATc4 was observed to be localized mainly in the retinal ganglion cells (RGCs). In addition, the expression patterns of active caspase-3, active caspase-8, and FasL were parallel with that of NFATc4. We also found the co-localization of NFATc4 with active caspase-3 and FasL in RGCs after light exposure. Collectively, we hypothesized that NFATc4 might participate in RGCs apoptosis by upregulating FasL levels.
More Related Videos
04:02Author Spotlight: Developing Precise and Clinically Relevant Models for Studying Secondary Degeneration in Traumatic Optic Neuropathy
Published on: November 29, 2024
06:27Müller Glia Cell Activation in a Laser-induced Retinal Degeneration and Regeneration Model in Zebrafish
Published on: October 27, 2017