Small RNA-seq of Extraceullular Vesicles derived from human immortalized podocytes treated with glucose and RabGTPase silenced

ABSTRACT: Diabetic nephropathy (DN) is a major cause of end-stage renal disease and is characterized by early podocyte injury, leading to progressive glomerular dysfunction. Increasing evidence highlights extracellular vesicles (EVs) as crucial mediators of intercellular communication in the diabetic kidney, transferring bioactive molecules such as non-coding RNAs (ncRNAs) that modulate cellular responses and contribute to disease progression. The molecular mechanisms governing the selective packaging of ncRNAs into podocyte-derived EVs under hyperglycaemic stress, as well as the role of vesicle trafficking regulators such as RAB GTPases, remain poorly understood. In this study, conditionally immortalized human podocytes were exposed to high glucose conditions to model the diabetic environment. To investigate the contribution of vesicular trafficking to EV release, the small GTPases RAB27A and RAB3A were silenced using siRNA. EVs were isolated and their small RNA content was profiled by next-generation sequencing followed by RT-qPCR validation. The results demonstrated that both hyperglycaemia and RAB GTPase knockdown significantly modified the ncRNA composition of podocyte-derived EVs, indicating that glucose stress and vesicular trafficking pathways jointly shape the extracellular RNA landscape. These findings provide new insights into how RAB GTPase–dependent mechanisms regulate EV-mediated communication in podocytes during diabetic injury, potentially influencing key signaling pathways involved in disease progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE310639 | GEO | 2026/04/16

REPOSITORIES: GEO