Regulation by estrogen of synthesis and secretion of apolipoprotein A-I in the chicken hepatoma cell line, LMH-2A

• Published in: Biochimica et biophysica acta 2003-06, Vol.1641 (1), p.25-33
• Main Authors: Hermann, Marcela, Foisner, Roland, Schneider, Wolfgang J., Ivessa, N.Erwin
• Format: Article
• Language: English
• Subjects: Animals; Apolipoprotein A-I; Apolipoprotein A-I - biosynthesis; Apolipoproteins B - biosynthesis; Apolipoproteins B - blood; Apolipoproteins B - chemistry; Cell Line; Chickens; Estrogens - pharmacology; Ethinyl Estradiol - analogs & derivatives; Ethinyl Estradiol - pharmacology; Female; Gene Expression Regulation, Neoplastic; High-density lipoprotein; Hormonal regulation; Kinetics; Lipoproteins, HDL - blood; Lipoproteins, HDL - chemistry; Liver Neoplasms, Experimental - metabolism; Male; Secretory pathway; Very low density lipoprotein
• ISSN: 0167-4889; 0006-3002; 1879-2596
• DOI: 10.1016/S0167-4889(03)00046-6

The synthesis and secretion of apolipoprotein A-I (apoA-I) in response to the treatment with estrogen were investigated in the chicken hepatoma cell line, LMH-2A. Exposure of these cells to exogenous estrogen for up to 48 h results in a decrease of apoA-I production, as evident from Western blotting, immunoprecipitation, and immunofluorescence experiments. Likewise, the secretion of apoA-I is also decreased in estrogen-treated cells when compared to controls. However, under both conditions, the disappearance of the apoprotein from the cells occurs very rapidly and with similar kinetics. The bulk of apoA-I secreted from LMH-2A cells is recovered on lipoprotein particles with a buoyant density of ≥1.10 g/ml, corresponding to HDL and heavy LDL. Interestingly, apoA-I is detectable on apoB-containing lipoproteins by sequential immunoprecipitation, suggesting that the two apoproteins co-reside at least on a subfraction of the secreted particles, or that apoB- and apoA-I-containing particles interact. These interactions are more pronounced in estrogen-treated cells, most likely due to the dramatic estrogen-mediated induction of apoB synthesis and secretion.