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Decreased transcription, expression and function of low-density lipoprotein receptor in leukocytes from patients with systemic lupus erythematosus.

机译:系统性红斑狼疮患者白细胞中低密度脂蛋白受体的转录,表达和功能降低。

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摘要

The low-density lipoprotein receptor (LDLR) is directly involved in the metabolism of low-density lipoprotein (LDL) and its impairment causes accumulation of plasmatic LDL leading to atherosclerosis, a prevalent disease in patients with systemic lupus erythematosus (SLE). We studied LDLR transcription, expression and function in leukocytes patients with SLE and normal healthy donors (NHD). The ratio LDLR/glyceraldehyde-3-phosphate dehydrogenase (GADPH) mRNAs the expression of LDLR and the uptake of LDL-DiI were significantly lower (p < 0.001) in the patients with SLE. On the contrary, patients with SLE had significantly higher (p < 0.0001) levels of total cholesterol, LDL cholesterol and anti-oxLDL autoantibodies (AAb) as compared to NHD. No correlation between LDLR transcription, expression and function with the SLE disease activity index or with treatment was found. The decreased function of LDLR was independent of treatment. It seems dependent on the sterol regulatory binding protein and may be responsible for the increase of plasma LDL cholesterol and oxLDL AAb further increasing the risk of vascular diseases.
机译:低密度脂蛋白受体(LDLR)直接参与低密度脂蛋白(LDL)的代谢,其损害会导致血浆LDL积累,从而导致动脉粥样硬化,这是系统性红斑狼疮(SLE)患者的普遍疾病。我们研究了患有SLE和正常健康捐献者(NHD)的白细胞患者的LDLR转录,表达和功能。 SLE患者的LDLR /甘油醛-3-磷酸脱氢酶(GADPH)mRNA比率,LDLR表达和LDL-DiI摄取显着降低(p <0.001)。相反,与NHD相比,SLE患者的总胆固醇,LDL胆固醇和抗oxLDL自身抗体(AAb)的水平明显更高(p <0.0001)。 LDLR转录,表达和功能与SLE疾病活动指数或治疗之间无相关性。 LDLR的功能下降与治疗无关。它似乎依赖于固醇调节结合蛋白,可能与血浆LDL胆固醇和oxLDL AAb的增加有关,进一步增加了患血管疾病的风险。

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