Poster #082
Endothelial AGO1 Targeting Protects from Diabetes-Induced β Damage
Mentor: Alonso Tapia, Grad Student
The pancreas contains clusters of cells, islets, which regulate blood sugar by secreting hormones like insulin. Islets rely on endothelial cells (ECs), which form blood vessels that support function. Our previous work demonstrated Argonaute 1 (AGO1) as a key regulator of endothelial function and its suppression in ECs confers an anti-obesity effect. However, the role of endothelial AGO1 in the islet function is unknown. We hypothesize that AGO1 inhibition in ECs can protect islets from damage in a diabetes model. We used genetically modified mice lacking AGO1-specifically in ECs (EC-AGO1-KO) and induced β-cell injury by injecting Streptozotocin (STZ). We then examined pancreas sections with immunostaining to detect cell proliferation (Ki67) and apoptosis (TUNEL). Results showed EC-AGO1-KO mice had increased proliferation and reduced inflammation compared to wild-type mice. Our study indicates that targeting EC-AGO1 could protect and restore islet function, offering potential new avenues for treatment strategies for management of diabetes.