The role of hepatitis B virus surface protein in inducing Sertoli cell ferroptosis

• DOI: 10.1111/andr.13520
• Publication Date: 2023-08-30T07:35:35Z
• Authors: Chengshuang Pan; Xiangbin Kong; Zhigang Wu; Qianjin Fei
• Keywords: Viability assay

Abstract Backgrounds Hepatitis B virus infection could result in male infertility with sperm defects and dysfunction. Sertoli cells are essential for testis function play a crucial role spermatogenesis. cell death contributes to spermatogenesis impairment, leading poor quality. Ferroptosis has been implicated as mechanism of death. The issue studying the relationship between hepatitis ferroptosis not yet addressed. Objectives To explore mechanisms underlying virus‐exposed cells. Materials methods Human were treated vitro levels 25, 50, 100 μg/mL surface protein (HBs). Cell viability glutathione, malondialdehyde, cellular ferrous ion (Fe 2+ ), lipid peroxidation, N 6‐methyladenosine detected. level glutathione peroxidase 4, transferrin receptor 1, ferritin heavy chain, tripartite motif (TRIM) 37, methyltransferase like 3, insulin‐like growth factor 2 mRNA binding was examined. transfection carried out alter expression ferroptosis‐related proteins. qPCR immunoblotting performed measure level. Immunoprecipitation applied determine protein‐RNA interaction. Luminescence analysis identify target 3. Results HBs exposure triggered featured increased intracellular Fe ion, reduced 4 treatment significantly TRIM37 expression, which suppressed through ubiquitination. silencing attenuated effect exposure‐regulated ferroptosis. upregulated modification 3′‐UTR by increasing 3 expression. reader enhanced stability mRNA. Conclusion can decrease human promoting induced loss activity TRIM37‐mediated ubiquitination 4. findings highlight TRIM37/glutathione signaling responsible regulation virus‐infected