Open Access

ARTICLE

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

WENJUAN ZHU¹, ZHENGZHENG JU², FAN CUI^2,*

1 Department of Blood Transfusion, The First People’s Hospital of Wuhu, Wuhu, 241000, China
2 Department of Clinical Laboratory, The First People’s Hospital of Wuhu, Wuhu, 241000, China

* Corresponding Author: FAN CUI. Email:

BIOCELL 2024, 48(9), 1379-1388. https://doi.org/10.32604/biocell.2024.052205

Received 26 March 2024; Accepted 25 June 2024; Issue published 04 September 2024

Abstract

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.

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