Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk 712-714, Republic of Korea.
Biochem Biophys Res Commun. 2012 Apr 13;420(3):588-93. doi: 10.1016/j.bbrc.2012.03.038. Epub 2012 Mar 16.
Our previous proteomics study revealed that long chain acyl CoA synthetase 1 (ACSL1) and gelsolin (GSN) are oppositely regulated in white adipose tissue of diet-induced obese rats. To firmly establish these proteins as mediators of adipogenic and/or lipogenic events, we efficiently knocked down the Acsl1 and Gsn genes using siRNA in 3T3-L1 adipocyte cells. Expectedly, Acsl1 knockdown stimulated expression of lipogenic genes. Interestingly, Gsn knockdown suppressed expression of lipogenic genes but strikingly increased that of Tnfα and Il6, which may have connections with lipolytic capacity of these genes. Conclusively, we provide clear evidence that ACSL1 and GSN are potential target proteins in the context of obesity.
我们之前的蛋白质组学研究表明,长链酰基辅酶 A 合成酶 1(ACSL1)和凝溶胶蛋白(GSN)在饮食诱导肥胖大鼠的白色脂肪组织中呈相反调节。为了将这些蛋白确定为脂肪生成和/或脂肪生成事件的介质,我们使用 siRNA 在 3T3-L1 脂肪细胞中有效地敲低了 Acsl1 和 Gsn 基因。预期地,ACSL1 敲低刺激了脂肪生成基因的表达。有趣的是,GSN 敲低抑制了脂肪生成基因的表达,但显著增加了 Tnfα 和 Il6 的表达,这可能与这些基因的脂肪分解能力有关。总之,我们提供了明确的证据表明 ACSL1 和 GSN 是肥胖背景下的潜在靶蛋白。