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首页> 外文期刊>Biochemistry >Adenovirus-Mediated Expression of Caveolin-1 in Mouse Liver Increases Plasma High-Density Lipoprotein Levels
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Adenovirus-Mediated Expression of Caveolin-1 in Mouse Liver Increases Plasma High-Density Lipoprotein Levels

机译：腺病毒介导的小鼠肝脏Caveolin-1表达增加血浆高密度脂蛋白水平

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Caveolae are 50-100 nm plasma membrane invaginations, which function in cell signaling and transcytosis, as well as in regulating cellular cholesterol homeostasis. These subcompartments of the plasma membrane are characterized by the presence of caveolin proteins. Recent studies have indicated that caveolae may be involved in the regulation of cellular cholesterol efflux to HDL, as well as selective uptake mediated by SR-BI. In the present study, we have determined the effect of caveolin-1 overexpression in mouse liver on plasma lipoprotein metabolism. We evaluated this effect using an adenovirus-mediated gene delivery system. C57BL/6J mice were injected with adenoviruses encoding either caveolin-1 (Adcav-1) or green fluorescent protein (AdGFP) together with a transactivator adenovirus (AdtTA). We found that, after adenovirus injection, caveolin-1 was overexpressed in hepatocytes. Moreove, the recombinant protein was localized to the plasma membrane. We also found that caveolin-1 overexpressing animals, plasma HDL-cholesterol levels were found to be approx2-fold elevated, as compared with control animals. To determine the effect of caveolin-1 on SR-BI-mediated selective uptake, we infected murine hepatocytes in culture with an adenoviral vector carrying the caveolin-1 cDNA or GFP as a control protein. We show that, in primary cultures of hepatocytes, caveolin-1 inhibits DiI-HDL uptake mediated by SR-BI. This result would mechanistically expain the increased plasma HDL-cholesterol levels we observed in caveolin-1 adenovirus-injected nimals. In addition, caveolin-1 expression increased the secretion of apolipoprotein A-I in cultured hepatocytes and increased apolipoprotein A-I plasma levels in mice. Our study therefore demonstrates an important role for caveolin-1 in regulating HDL metabolism.
机译：小窝是50-100 nm的质膜内陷，在细胞信号传导和胞吞作用以及调节细胞胆固醇稳态中起作用。质膜的这些小室的特征在于小窝蛋白的存在。最近的研究表明，小窝蛋白可能参与细胞胆固醇向HDL的外流调节，以及SR-BI介导的选择性摄取。在本研究中，我们确定了小鼠肝脏中小窝蛋白1过表达对血浆脂蛋白代谢的影响。我们使用腺病毒介导的基因递送系统评估了这种效果。 C57BL / 6J小鼠注射了编码小窝蛋白-1（Adcav-1）或绿色荧光蛋白（AdGFP）的腺病毒以及反式激活腺病毒（AdtTA）。我们发现，腺病毒注射后，caveolin-1在肝细胞中过表达。此外，重组蛋白位于质膜上。我们还发现，与对照动物相比，caveolin-1过表达的动物血浆HDL-胆固醇水平升高了约2倍。为了确定小窝蛋白-1对SR-BI介导的选择性摄取的影响，我们用携带小窝蛋白-1 cDNA或GFP作为对照蛋白的腺病毒载体感染了培养的鼠肝细胞。我们显示，在肝细胞的原代培养中，caveolin-1抑制由SR-BI介导的DiI-HDL摄取。该结果将机械地解释我们在注射cavolin-1腺病毒的动物中观察到的血浆HDL-胆固醇水平升高。此外，caveolin-1的表达增加了培养的肝细胞中载脂蛋白A-1的分泌，并增加了小鼠载脂蛋白A-1的血浆水平。因此，我们的研究表明小窝蛋白1在调节HDL代谢中的重要作用。

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