SOX4 promotes high-glucose-induced inflammation and angiogenesis of retinal endothelial cells by activating NF-κB signaling pathway

Abstract

Abstract Diabetic retinopathy (DR) is a type of main microvascular complication of diabetes mellitus (DM) and an important factor that causes blindness in adults. SOX4 is a transcription factor expressed in the pancreas and is essential for normal endocrine pancreatic development. However, the effect and the regulatory mechanism of SOX4 on DR have not been reported. In the present study, upregulation of SOX4 was found in DM patients, particularly in DR patients and mice models. The in vitro experiments showed that SOX4 depletion increased the viability and inhibited the inflammation level of human retinal endothelial cells (HRCECs) induced by high glucose. Besides, SOX4 knockdown inhibited the migration and angiogenesis of HRCECs upon high glucose treatment. Mechanically, depletion of SOX4 inhibited the NF-κB pathway. Therefore, SOX4 could serve as a promising target for DR treatment.