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Title: [Effects of oxidized low-density lipoprotein on cholesterol efflux in 3T3-L1 cells]. Author: Yu BL, Zhao SP, Xie XZ, Dong SZ, Dong J. Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2007 Aug; 32(4):631-6. PubMed ID: 17767055. Abstract: OBJECTIVE: To explore whether oxidized low-density lipoprotein (ox-LDL) can stimulate the cholesterol efflux in fully differentiated 3T3-L1 cells and the possible mechanism. METHODS: Fully differentiated 3T3-L1 cells were incubated in the medium containing various concentrations of ox-LDL ( 0 to 50 microg/mL) for 8 or 24 hours. 22(R)-Hydroxycholesterol (10 micromol/L) was exposed to preconditioned adipocytes with 25 microg/mL ox-LDL for 24 hours. Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate ATP binding cassette transporter A1 (ABCA1), scavenger receptor class B type I (SR-BI), and liver X receptor alpha (LXRalpha) mRNA expression. Cholesterol efflux mediated by apolipoprotein A-I (apoA-I) was determined using liquid scintillator. RESULTS: Low levels (12.5-25 microg/mL) of ox-LDL could increase cholesterol efflux via the enhancement of ABCA1 pathway and SR-BI expression, whereas the higher concentration (50 microg/mL) could not. In adipocytes preincubated with 25 microg/mL ox-LDL for 24 hours, 22(R)-hydroxycholesterol could increase ABCA1 and LXRalpha mRNA and apoA-I-mediated cholesterol efflux, but had no effect on the SR-BI mRNA expression. CONCLUSION: Low levels of ox-LDL may enhance the LXRalpha-ABCA1-apoA-I pathway in adipocytes, up-regulate SR-BI mRNA expression, and then increase the cholesterol efflux. This new effect of ox-LDL will not only make contribution to cholesterol homeostasis in adipocytes, but also be potentially atheroprotective.[Abstract] [Full Text] [Related] [New Search]