Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Mar;200(3):1127-1139.
doi: 10.1007/s12011-021-02730-1. Epub 2021 Apr 24.

Selenium Deficiency Leads to Changes in Renal Fibrosis Marker Proteins and Wnt/β-Catenin Signaling Pathway Components

Tingting Lin #  1 , Jiaqi Tao #  1 , Ying Chen  1 , Yitong Zhang  1 , Fenglan Li  1 , Yutong Zhang  1 , Xueqing Han  1 , Zihui Zhao  1 , Guiyan Liu  1 , Hui Li  2
Affiliations

Selenium Deficiency Leads to Changes in Renal Fibrosis Marker Proteins and Wnt/β-Catenin Signaling Pathway Components

Tingting Lin et al. Biol Trace Elem Res. 2022 Mar.

Abstract

Renal fibrosis is the final result of the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD). Earlier studies confirmed that selenium (Se) displays a close association with kidney diseases. However, the correlation between Se and fibrosis has rarely been explored. Thus, this article mainly aimed to investigate the effect of Se deficiency on renal fibrosis and the Wnt/β-catenin signaling pathway. Twenty BALB/c mice were fed a diet containing 0.02-mg/kg Se (Se-deficient diet) or 0.18-mg/kg Se (standard diet) for 20 weeks. A human glomerular mesangial cell (HMC) cell line was transfected with lentiviral TRNAU1AP-shRNA vector to establish a stable Se deficiency model in vitro. As indicated in this study, the glutathione (GSH) content in the Se-deficient group displayed an obvious decline compared with that in the control group, whereas the content of malondialdehyde (MDA) was obviously elevated. The results of Masson staining showed fibrosis around the renal tubules, and the results of immunohistochemistry showed that the area of positive fibronectin expression increased. In the Se-deficient group, the levels of collagen I, collagen III, matrix metalloproteinase 9 (MMP9), and other fibrosis-related proteins changed significantly in vivo and in vitro. Compared with the control group, the TRNAU1AP-shRNA group showed markedly reduced cell proliferation and migration abilities. Our data indicate that Se deficiency can cause kidney damage and renal fibrosis. Furthermore, the Wnt pathway is critical for the development of tissue and organ fibrosis. The data of this study demonstrated that the expression of Wnt5a, β-catenin, and dishevelled 1 (Dvl-1) was significantly upregulated in the Se-deficient group. Therefore, the Wnt/β-catenin pathway may play an important role in renal fibrosis caused by Se deficiency.

Keywords: Oxidative stress; Renal fibrosis; Se deficiency; Selenoprotein; Wnt/β-catenin.

PubMed Disclaimer

References

    1. Schwarz K, Foltz CM (1999) Selenium as an integral part of factor 3 against dietary necrotic liver degeneration. Nutrition 15:255 - PubMed
    1. Lu J, Holmgren A (2009) Selenoproteins. J Biol Chem 284:723–727 - PubMed
    1. Zachara BA (2015) Selenium and selenium-dependent antioxidants in chronic kidney disease. Adv Clin Chem 68:131–151 - PubMed
    1. Kilinc M, Guven MA, Ezer M, Ertas IE, Coskun A (2008) Evaluation of serum selenium levels in Turkish women with gestational diabetes mellitus, glucose intolerants, and normal controls. Biol Trace Elem Res 123:35–40 - PubMed
    1. Zhou H, Wang T, Li Q, Li D (2018) Prevention of Keshan disease by selenium supplementation: a systematic review and meta-analysis. Biol Trace Elem Res 186:98–105 - PubMed

LinkOut - more resources