Menglu Yang, MD, PhD, Investigator, Schepens Eye Research Institute, Harvard Medical School
Electrifying Solutions: Microcurrent Stimulation for Corneal Nerve Regeneration
Date: Thursday, October 30th, 2025
Time: 10:00am ET
Location: 4001 Pelotonia Research Center (in person with zoom option)
ABSTRACT. Purpose: Diabetes mellitus (DM) is a chronic metabolic disorder that poses a significant global health challenge. Diabetic neuropathy (DN) is a common complication of DM characterized by distal-to-proximal loss of nerve function and density. As the most innervated tissue of the body, the cornea is often involved, namely diabetic keratopathy (DK). Transcuta, Harv,neous electrical stimulation (TES) is a neural modulating therapy that non-invasively delivers microcurrent electricity to the eye via orbital skin. This study investigates the neural regenerative potential of TES in a type I DM model and delves into the molecular events of electrical-induced neural regeneration. Result: DK was induced in adult C57BL6J mice at 15 weeks post-STZ. Following the 2-week TES treatment, the TES ameliorated the corneal epithelial damage associated with DK, increased the plexus density, contrasting with decreased density and disrupted structure in the sham control. Isolated trigeminal ganglia (TG) neurons from the TES group displayed significantly longer neurites than sham controls, indicative of the direct neuronal stimulation effect of the TES. Bulk RNASeq revealed an up-regulated expression in ion transport and Ca2+ signaling by ES, was well as the Ca2+-regulated gene repressor Kcnip3. The membrane potential recording of isolated TG upon ES showed a sudden hyperpolarization, in combination with increased intracellular Ca2+ level, both can be opposed by the removal of Ca2+. Chemical blocker of Ca2+-Induced K+ Channel (KCNN), Apamin, abolished the neural regeneration process induced by electrical stimulation in trigeminal ganglia which innervates the cornea in both primary TG culture and in keratectomy model, while KCNN channel agonist NS309 significantly increased the neural regeneration marker growth-associated protein 43 (GAP43) in STZ model compared to sham treatment. Conclusion: TES effectively restores corneal nerve density and protects the corneal epithelium in a type I DM model by activating KCNN channels.
BIO. Dr. Yang’s research interests lie in the resolution of inflammation, and the inflammasome pathways of ocular surface diseases. She was trained as a postdoctoral fellow at Schepens Eye Research Institute of Mass Eye and Ear, during which time she elucidated the cellular signaling pathways that specialized pro-resolving mediators use to inhibit the action of proinflammatory mediators in the conjunctival goblet cells. Her current research is focused on the mechanism of inflammasome activation of lacrimal glands during the onset of Sjögren Syndrome. Dr. Yang holds a medical degree from Peking University, where she completed residency training in the field of ophthalmology and was awarded as the Merit Student of Peking University.
All OSU investigators with an interest in vision sciences research are invited to attend.