Sodium-dependent regulation and immune cell infiltration is mediated by YB-1

Y-box binding protein-1 exerts pleiotropic functions in cells through its ability to bind single-stranded RNA and/or DNA. Thereby, it regulates immune cell phenotypes and inflammatory processes induced by cellular stress. YB-1 also binds to specific cell surface receptors, affecting cell proliferation and migration. High salt intake is one of the major causes leading to hypertension, and a high salt environment within the body can enhance the inflammatory response. In the body, blood pressure is regulated by renin-angiotensin-aldosterone-system (RAAS) and sodium reabsorption. The sensitivity of salt influences the effect of high salt intake on blood pressure. Since homozygous Ybx1 knockout animals are embryonic lethal, Tamoxifen was used to induced knockout of the Ybx1 gene in 3-month-old C57BL/6J/N mice. By knocking out the Ybx1 gene in C57BL/6J/N mice, the mice survived, and the measured physiological indexes were similar to those of wild type mice. Under a high salt diet, inflammatory response in YB-1 knockout mice is reduced. The immuncell numbers in YB-1 knockout mice with high salt diet are reduced to the same level als normal salt diet wild type mice. The experiment found that C57BL/6J/N mice are salt-tolerant strains, 4% NaCl feeding does not cause hypertension, but the absence of YB-1 gene has been shown to have a certain effect on the decline of systolic blood pressure. The measured physiological indicators by YB-1 knockout mice after high salt diet were similarly to those of normal salt diet wild type mice, demonstrating that the deletion of the YB-1 gene can protect mice from the negative impact of high salt intake.