new insights

Little regulatory molecules called micro-RNAs are essential for proper maturation, composition, and function in the postnatal retina.

In our recent study published in iScience, we show that altering the molecular composition in immature cells during retinal development results in delays of retinal cell maturation in the developing eye after birth. Specifically, we removed a molecule called Dicer, which produces many small genetic regulators known as microRNAs. These regulators help cells to develop into the right cell types at the right time. When Dicer was removed from these developing retinal cells, the retina did not form properly. In adult eyes, the light-sensing rod cells did not function well, and there were fewer support cells (Müller glia). Interestingly, there was an overproduction of another neuron type called amacrine cells. They are normally born a little earlier, and it appears that their development is regulated by the miRNAs miR-25/20. We also found that some young retinal cells never fully matured and stayed “immature”, i.e., remained stuck in an early developmental stage, even into adulthood. This shows that Dicer and microRNAs are essential for proper retinal cell maturation, so a healthy, functioning retina can form. Our data also shows that miRNAs play a role in Müller glia maturation, hence they can probably be used to rejuvenate these cells for therapeutic purposes.

Why is it important to know that miRNAs play a role in retinal development? Well, knowing which specific miRNAs are regulating a specific cell type will help to develop better tools for endogenous cell reprogramming or for organoid research, two current promising strategies in regenerative medicine to restore lost neurons in patients.

Kang, S., Larbi, D., Bruns, E., Hahne, K., Khodadadi-Jamayran, A., Sreenivasaiah, C., Lima Carneiro, M., Andrade, M., Batsuuri, K., Chen, S., Jager, J., Viswanathan, S., Clark, B.S., Wohl, S. G. 2025. “Dicer is essential for proper maturation, composition, and function in the postnatal retina.” iScience, 28, 113794.

Müller glia ensure proper cone Photoreceptor function and therefore ensure color vision

In another recent study published in IOVS, we show that altering the molecular composition in young Muller glia results in the loss of their physiological, essential properties. The first affected neuron type is cone photoreceptors, which are required for color vision. When we removed a key enzyme called Dicer, which helps produce small gene regulators (microRNAs), the cones began to lose their structure and function. Over time, the damage progressed and resulted in severe retinal degeneration.

This study shows that Müller glia are not just passive support cells, but essential key elements critical for maintaining healthy vision. Importantly, we demonstrate for the first time that malfunctioning Müller glia alone can trigger retinal degeneration that resembles diseases such as retinitis pigmentosa or dry age-related macular degeneration.

Why is that important to know? Well, understanding that specific microRNAs are necessary to keep glial cells functioning properly reveals a new possible cause of retinal disease. Instead of focusing only on damaged neurons, we now see that problems in support cells can start the disease process. This opens the door to new treatment strategies aimed at restoring the normal balance of microRNAs in glial cells. By doing so, we may be able to slow disease progression and delay vision loss.

Larbi, D., Rief, A.M., Kang, S., Chen, S., Batsuuri, K., Fuhrmann, S., Viswanathan, S., Wohl, S. G., 2025. Dicer Loss in Muller Glia Leads to a Defined Sequence of Pathological Events Beginning With Cone Dysfunction. Invest Ophthalmol Vis Sci, 66, 7.