Complement inhibitory proteins expression in placentas of thrombophilic women

Folia Histochem Cytobiol. 2012 Oct 8;50(3):460-7. doi: 10.5603/19758.

Abstract

Factors controlling complement activation appear to exert a protective effect on pregnancy. This is particularly important in women with thrombophilia. The aim of this study was to determine the transcript and protein levels of complement decay-accelerating factor (DAF) and membrane cofactor protein (MCP) in the placentas of women with acquired and inherited thrombophilia. Also, we assessed immunohistochemistry staining of inhibitors of the complement cascade, DAF and MCP proteins, in the placentas of thrombophilic women.Placentas were collected from eight women with inherited thrombophilia and ten with acquired thrombophilia.The levels of DAF and MCP transcripts were evaluated by qPCR, the protein level was evaluated by Western blot. We observed a higher transcript (p < 0.05) and protein (p < 0.001) levels of DAF and MCP in the placentas of thrombophilic women than in the control group. DAF and MCP were localized on villous syncytiotrophoblast membranes, but the assessment of staining in all groups did not differ. The observed higher expression level of proteins that control activation of complement control proteins is only seemingly contradictory to the changes observed for example in the antiphospholipid syndrome. However, given the hitherto known biochemical changes associated with thrombophilia, a mechanism in which increased expression of DAF and MCP in the placentas is an effect of proinflammatory cytokines, which accompanies thrombophilia, is probable.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Blotting, Western
  • CD55 Antigens / genetics
  • CD55 Antigens / metabolism*
  • Case-Control Studies
  • Female
  • Gene Expression Regulation
  • Humans
  • Immunohistochemistry
  • Membrane Cofactor Protein / genetics
  • Membrane Cofactor Protein / metabolism*
  • Placenta / metabolism*
  • Pregnancy
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Thrombophilia / metabolism*

Substances

  • CD46 protein, human
  • CD55 Antigens
  • Membrane Cofactor Protein
  • RNA, Messenger