BTG2 interference ameliorates high glucose-caused oxidative stress, cell apoptosis, and lipid deposition in HK-2 cells

Objective: Diabetic nephropathy (DN) is a deleterious microangiopathy of diabetes, constituting a critical determinant of fatality in diabetic patients.This work is purposed to disclose the effects and modulatory mechanism of BTG anti-proliferation factor 2 (BTG2) during the pathological process of DN.Methods: BTG2 expression in kidney tissues of diabetic mice and high glucose (HG)-exposed human proximal tubular cell line HK-2 was assessed with Western blot and RT-qPCR.The diabetic mice model was constructed by streptozotocin injection and confirmed by the blood glucose level beyond 16.7 mmol/L.Hematoxylin and eosin (H&E) staining and measurement of kidney function hallmarks were conducted to assess kidney injury.Cell counting kit (CCK)-8 method and TUNEL assay appraised cell activity and apoptosis.Oil red O staining assayed lipid accumulation.Relevant commercial kits were used to estimate oxidative stress-related factors.Co-immunoprecipitation (Co-IP) assay testified the binding relationship of BTG2 with protein arginine methyltransferase 1 (PRMT1).Results: BTG2 expression was significantly raised in renal tissues of diabetic mice and HK-2 cells exposed to HG. BTG2 deficiency improved viability and extenuated the apoptosis, lipid deposition as well as oxidative stress in HK-2 cells following HG exposure.In addition, PRMT1 was also overexpressed in HK-2 cells exposed to HG. BTG2 interacted with PRMT1 and positively modulated PRMT1 expression.The effects of BTG2 interference on viability, apoptosis, lipid deposition, and oxidative stress in HG-challenged HK-2 cells were partially abrogated by PRMT1 overexpression.Conclusion: Altogether, BTG2 might aggravate HK-2 cell injury in response to HG by binding with PRMT1, providing a novel target for the therapeutic strategy of DN.