PMID: 8443235Feb 24, 1993Paper

Effect of VLDL on the inhibition of arachidonic acid transformation by dexamethasone in cultured smooth muscle cells

Biochimica Et Biophysica Acta
I E PetrichenkoY u Shakhov

Abstract

Very-low-density lipoproteins (VLDL) induce a dose-dependent reduction (up to 55%) in the number of specific binding sites and about a 2-fold increase in binding affinity for [3H]dexamethasone in human and rat smooth muscle cells (SMC). Maximal effect of VLDL was achieved within 3-5 h at a lipoprotein concentration 60 micrograms protein/ml. Lipoprotein-mediated reduction in the number of [3H]dexamethasone binding sites resulted in partial loss of cellular sensitivity to hormone action: dexamethasone (1 x 10(-6) M) inhibited the transformation of [14C]arachidonic acid (AA) into metabolites to a lesser extent in SMC preincubated with VLDL (11.5%) than in untreated cells (29.0%). In particular, under these conditions the inhibitory effect of dexamethasone on prostaglandin I2 (PGI2) formation in VLDL-treated SMC was lower than in untreated cells (42.1% vs. 60%). We propose that VLDL is able to counteract the inhibitory effect of glucocorticoids on AA release and PGI2 formation in vascular SMC by reduction of cellular specific glucocorticoid binding sites.

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Citations

Dec 23, 2006·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Shuichi ItoShumpei Yokota
Jan 5, 2008·Clinical and Experimental Nephrology·Shuzo Kobayashi
Dec 5, 2003·American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation·Motoshi HattoriKatsumi Ito
Jun 1, 1997·Arteriosclerosis, Thrombosis, and Vascular Biology·I E PetrichenkoJ Larrue
Oct 7, 2011·Therapeutic Apheresis and Dialysis : Official Peer-reviewed Journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy·Satoshi UedaTsukasa Takemura

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