Instituto de Fisiología Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, 2000, Rosario, Santa Fe, Argentina.
Instituto de Fisiología Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, 2000, Rosario, Santa Fe, Argentina.
Biochimie. 2021 Sep;188:16-19. doi: 10.1016/j.biochi.2021.01.008. Epub 2021 Jan 23.
We recently provided evidence suggesting that mitochondrial aquaporin-8 (mtAQP8), a channel protein able to conduct HO, is involved in the modulation of hepatocyte cholesterogenesis. To expand that study, we cultured human hepatocyte-derived Huh-7 cells in medium with lipoprotein-deficient serum (LPDS) to induce the de novo synthesis of cholesterol and fatty acids. We found that LPDS induced mtAQP8 expression and that AQP8 gene silencing significantly down-regulated the LPDS-induced synthesis of cholesterol and fatty acids as well as the expression of the corresponding key biosynthetic enzymes, 3-hydroxy-3-methylglutaryl-CoA reductase and fatty acid synthase. Our data further support a regulatory role of mtAQP8 in hepatocyte lipid homeostasis.
我们最近提供的证据表明，线粒体水通道蛋白-8（mtAQP8）是一种能够传导 HO 的通道蛋白，参与调节肝细胞胆固醇生成。为了扩展该研究，我们在含有脂蛋白缺乏血清（LPDS）的培养基中培养人源性肝细胞系 Huh-7 细胞，以诱导胆固醇和脂肪酸的从头合成。我们发现 LPDS 诱导 mtAQP8 的表达，AQP8 基因沉默显著下调 LPDS 诱导的胆固醇和脂肪酸的合成以及相应关键生物合成酶 3-羟-3-甲基戊二酰辅酶 A 还原酶和脂肪酸合酶的表达。我们的数据进一步支持 mtAQP8 在肝细胞脂质稳态中的调节作用。
