title: Reciprocal coordination of a combination oral contraceptive containing desogestrel+ethinyl estradiol on the expression of LOX-1 and LDLR in placental trophoblast cells.
abstract: BACKGROUND
  The aim of this study was to assess the consistency of antiatherosclerotic potential of a combination oral contraceptive steroid (ethinyl estradiol+desogestrel) by rating its effect on the differential expression of the low-density lipoprotein receptor (LDLR) and lectin-like oxidized LDL (LOX-1) receptor.
  
  
  METHODS
  Cells from placental trophoblast cell line (JAR) and differentiated primary placental trophoblast cells isolated from term human placentae were used for this study. Expressions of LOX-1 and LDLR were assessed by immunoblot and immunocytochemistry assays. Differential effects of the constituent steroids in the combination of ethinyl estradiol and desogestrel were verified on the expression profile of the receptors.
  
  
  RESULTS
  Desogestrel opposed the effect of ethinyl estradiol on LOX-1 expression, and when used in combination, the combination oral contraceptive reduced the expression of LOX-1 in contrast to LDLR. The characteristic change in the expressions of LOX-1 and LDLR showed an antiatherosclerotic improvisation at the unique combination of ethinyl estradiol (10 ng/mL) and desogestrel (20 ng/mL).
  
  
  CONCLUSIONS
  The aforesaid combination of ethinyl estradiol and desogestrel keeps LOX-1 and LDLR reciprocally expressed in antiatherosclerotic mode.
authors.affiliation: Department of Biochemistry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi-110 029, India.
authors.forename: Hemlata
authors.initials: H
authors.lastname: Pandey
authors.forename: Albina
authors.initials: A
authors.lastname: Arjuman
authors.forename: Kallol K
authors.initials: KK
authors.lastname: Roy
authors.forename: Nimai Chand
authors.initials: NC
authors.lastname: Chandra
mesh_terms: D050197:Atherosclerosis / Q000139:chemically induced / Q000517:prevention & control; D002460:Cell Line; D002478:Cells, Cultured; D003277:Contraceptives, Oral, Combined / Q000009:adverse effects / Q000494:pharmacology*; D003278:Contraceptives, Oral, Hormonal / Q000009:adverse effects / Q000494:pharmacology; D003280:Contraceptives, Oral, Synthetic / Q000009:adverse effects / Q000494:pharmacology; D017135:Desogestrel / Q000009:adverse effects / Q000494:pharmacology*; D015536:Down-Regulation / Q000187:drug effects; D004997:Ethinyl Estradiol / Q000009:adverse effects / Q000494:pharmacology*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000009:adverse effects / Q000494:pharmacology; D011257:Pregnancy Proteins / Q000378:metabolism*; D011973:Receptors, LDL / Q000378:metabolism*; D051127:Scavenger Receptors, Class E / Q000378:metabolism*; D014327:Trophoblasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D003277:Contraceptives, Oral, Combined; D003278:Contraceptives, Oral, Hormonal; D003280:Contraceptives, Oral, Synthetic; D000960:Hypolipidemic Agents; C495137:OLR1 protein, human; D011257:Pregnancy Proteins; D011973:Receptors, LDL; D051127:Scavenger Receptors, Class E; C442659:ethinyl estradiol-desogestrel combination; D004997:Ethinyl Estradiol; D017135:Desogestrel