In cultured HRMECs, ULMW-HA induced cell migration, whereas apigenin attenuated shedding of soluble syndecan-1 induced by diabetic mimetic conditions and reduced TNF-α-induced upregulation of ICAM-1, VCAM-1 and adherence of monocytes.<h4>Conclusions</h4>Abnormal HA metabolism is involved in diabetes-induced retinal endothelial dysfunction and ULMW-HA drives inflammation and angiogenesis in PDR. This evidence concerns the gene SDC1 and diabetes mellitus.