title: Altered autophagy induction by sera from pregnant women with pre-eclampsia: a case-control study.
abstract: OBJECTIVE
  Mechanisms leading to pre-eclampsia remain incompletely defined. Autophagy is a conserved process necessary for cell survival under adverse conditions. We hypothesised that sera from women with healthy pregnancies and women with pre-eclampsia differed in autophagy induction.
  
  
  METHODS
  A case-control study.
  
  
  METHODS
  Weill Cornell Medical College.
  
  
  METHODS
  Twenty-four normotensive pregnant women and 20 women with pre-eclampsia.
  
  
  METHODS
  Sera were incubated with peripheral blood mononuclear cells (PBMCs) from female donors. After 48 hours the PBMCs were lysed and the intracellular concentration of p62 was determined by enzyme-linked immunosorbent assay (ELISA). Its concentration is inversely proportional to the extent of autophagy induction. Serum endoglin, interleukin 13 (IL-13), insulin-like growth factor 1 (IGF-1), and transforming growth factor β1 (TGF-β1) levels were quantitated by ELISA.
  
  
  METHODS
  Differences in autophagy induction and serum mediator levels in the two groups.
  
  
  RESULTS
  Autophagy induction increased with gestational age in sera from normotensive women (P = 0.0045), but not in women with pre-eclampsia. In the presence of an autophagy inducer, the capacity for autophagy induction decreased with gestational age in sera from women with pre-eclampsia (P = 0.0235), but not from controls. Endoglin concentrations were positively associated with the extent of autophagy induction in controls only (P = 0.0141). There was no association between autophagy and serum IL-13, IGF-1, or TGF-β1 levels.
  
  
  CONCLUSIONS
  Sera from women with pre-eclampsia differ from normotensive women by their inability to induce autophagy as a function of gestational age.
authors.affiliation: Division of Immunology and Infectious Diseases, Department of Obstetrics and Gynecology, Weill Cornell Medical College, New York, NY, USA.
authors.forename: T T
authors.initials: TT
authors.lastname: Kanninen
authors.forename: A
authors.initials: A
authors.lastname: Jayaram
authors.forename: S
authors.initials: S
authors.lastname: Jaffe Lifshitz
authors.forename: S S
authors.initials: SS
authors.lastname: Witkin
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000097:blood*; D001343:Autophagy; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D000071063:Endoglin; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005865:Gestational Age; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D018793:Interleukin-13 / Q000097:blood*; D007963:Leukocytes, Mononuclear; D011225:Pre-Eclampsia / Q000097:blood / Q000503:physiopathology*; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000097:blood*; D053773:Transforming Growth Factor beta1 / Q000097:blood*
chemical_list: D015703:Antigens, CD; D015415:Biomarkers; C064206:ENG protein, human; D000071063:Endoglin; D018793:Interleukin-13; D011956:Receptors, Cell Surface; D053773:Transforming Growth Factor beta1; D007334:Insulin-Like Growth Factor I
keywords: Autophagy; endoglin; p62; pre-eclampsia; pregnancy; transforming growth factor β1