Complement inhibitory proteins expression in placentas of thrombophilic women

Factors controlling complement activation appear to exert a protective effect on pregnancy. This isparticularly important in women with thrombophilia. The aim of this study was to determine the transcript andprotein levels of complement decay-accelerating factor (DAF) and membrane cofactor protein (MCP) in theplacentas of women with acquired and inherited thrombophilia. Also, we assessed immunohistochemistry stainingof 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 Westernblot. We observed a higher transcript (p < 0.05) and protein (p < 0.001) levels of DAF and MCP in the placentasof thrombophilic women than in the control group. DAF and MCP were localized on villous syncytiotrophoblastmembranes, but the assessment of staining in all groups did not differ. The observed higher expression level ofproteins that control activation of complement control proteins is only seemingly contradictory to the changesobserved for example in the antiphospholipid syndrome. However, given the hitherto known biochemical changesassociated with thrombophilia, a mechanism in which increased expression of DAF and MCP in the placentas isan effect of proinflammatory cytokines, which accompanies thrombophilia, is probable.Factors controlling complement activation appear to exert a protective effect on pregnancy. This isparticularly important in women with thrombophilia. The aim of this study was to determine the transcript andprotein levels of complement decay-accelerating factor (DAF) and membrane cofactor protein (MCP) in theplacentas of women with acquired and inherited thrombophilia. Also, we assessed immunohistochemistry stainingof 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 Westernblot. We observed a higher transcript (p < 0.05) and protein (p < 0.001) levels of DAF and MCP in the placentasof thrombophilic women than in the control group. DAF and MCP were localized on villous syncytiotrophoblastmembranes, but the assessment of staining in all groups did not differ. The observed higher expression level ofproteins that control activation of complement control proteins is only seemingly contradictory to the changesobserved for example in the antiphospholipid syndrome. However, given the hitherto known biochemical changesassociated with thrombophilia, a mechanism in which increased expression of DAF and MCP in the placentas isan effect of proinflammatory cytokines, which accompanies thrombophilia, is probable