Han Sang Youb, Ghee Jung Yeon, Cha Jin Joo, Kang Young Sun, Kim Han Seong, Hur Dae Young, Cha Dae Ryong
Department of Internal Medicine, Inje University, Ilsan-Paik Hospital, Goyang 10380, Republic of Korea.
Department of Internal Medicine, Korea University, Ansan Hospital, Ansan 15355, Republic of Korea.
Life (Basel). 2023 Jan 19;13(2):277. doi: 10.3390/life13020277.
V-set Ig domain-containing 4 (VSIG4) regulates an inflammatory response and is involved in various diseases. However, the role of VSIG4 in kidney diseases is still unclear. Here, we investigated VSIG4 expression in unilateral ureteral obstruction (UUO), doxorubicin-induced kidney injury mouse, and doxorubicin-induced podocyte injury models. The levels of urinary VSIG4 protein significantly increased in the UUO mice compared with that in the control. The expression of VSIG4 mRNA and protein in the UUO mice was significantly upregulated compared with that in the control. In the doxorubicin-induced kidney injury model, the levels of urinary albumin and VSIG4 for 24 h were significantly higher than those in the control mice. Notably, a significant correlation was observed between urinary levels of VSIG4 and albumin (r = 0.912, < 0.001). Intrarenal VSIG4 mRNA and protein expression were also significantly higher in the doxorubicin-induced mice than in the control. In cultured podocytes, VSIG4 mRNA and protein expressions were significantly higher in the doxorubicin-treated groups (1.0 and 3.0 μg/mL) than in the controls at 12 and 24 h. In conclusion, VSIG4 expression was upregulated in the UUO and doxorubicin-induced kidney injury models. VSIG4 may be involved in pathogenesis and disease progression in chronic kidney disease models.
含V结构域免疫球蛋白4（VSIG4）可调节炎症反应，并参与多种疾病的发生。然而，VSIG4在肾脏疾病中的作用仍不清楚。在此，我们研究了VSIG4在单侧输尿管梗阻（UUO）、阿霉素诱导的肾损伤小鼠以及阿霉素诱导的足细胞损伤模型中的表达情况。与对照组相比，UUO小鼠尿中VSIG4蛋白水平显著升高。与对照组相比，UUO小鼠中VSIG4 mRNA和蛋白的表达显著上调。在阿霉素诱导的肾损伤模型中，24小时尿白蛋白和VSIG4水平显著高于对照小鼠。值得注意的是，尿中VSIG4水平与白蛋白之间存在显著相关性（r = 0.912，< 0.001）。阿霉素诱导的小鼠肾内VSIG4 mRNA和蛋白表达也显著高于对照组。在培养的足细胞中，阿霉素处理组（1.0和3.0μg/mL）在12小时和24小时时VSIG4 mRNA和蛋白表达显著高于对照组。总之，在UUO和阿霉素诱导的肾损伤模型中VSIG4表达上调。VSIG4可能参与慢性肾脏病模型的发病机制和疾病进展。
