Assessment of the transcription levels for the complement activation control system in eutopic endometrium in women with two or more consecutive miscarriages of unknown etiology.
Human endometrium, deciuda and placenta have been shown to express factors that inhibit the complement activation cascade - decay-accelerating factor (DAF), membrane cofactor protein (MCP) and the C3 complement component. In the following study we have analyzed the transcripts levels for DAF, MCP and heparin-binding epidermal growth factor-like growth factor (HB-EGF), the C3 complement component and receptor for vascular endothelial growth factor (VEGFR1) as markers of endometrial unbalance between factors activating the complement system in women with consecutive miscarriages. Study enrolled 30 women with at least two consecutive miscarriages, and 19 healthly women, that comprised the control group. RNA was isolated from endometrial samples. Transcripts levels of DAF and MCP was higher in women with consecutive miscarriages compared to controls, 0.78 vs 5.08 (p<0.001) and 0.25 vs 0.17 (p=0.001) respectively. In consecutive miscarriages group, DAF and MCP expression was correlated with the C3 expression, with r=0.60; p<0.001 and r= 0.40; p=0.03 respectively. Correlation between DAF and C3 was also noted in controls, 0.70; p=0.001. In women with two or more consecutive miscarriages the analysis proved higher expression of genes that encode proteins that inhibit the complement cascade. Further studies are needed to confirm that this might be a reaction to increased presence of the complement factors, which like C3 that are synthesized in the endometrium.
Division of Reproduction, Department of Obstetrics and Gynecology, K. Marcinkowski University of Medical Sciences, Poznań, Poland. abys@wp.pl
Przemysław
P
Wirstlein
Mateusz
M
Mikołajczyk
Jana
J
Skrzypczak
D000022:Abortion, Spontaneous / Q000209:etiology / Q000235:genetics*; D000328:Adult; D018958:CD55 Antigens / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D003167:Complement Activation / Q000235:genetics*; D003176:Complement C3 / Q000235:genetics / Q000378:metabolism; D003165:Complement System Proteins / Q000235:genetics / Q000378:metabolism; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D066257:Heparin-binding EGF-like Growth Factor; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism; D051916:Membrane Cofactor Protein / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D012313:RNA / Q000302:isolation & purification; D014158:Transcription, Genetic; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000378:metabolism
D018958:CD55 Antigens; D003176:Complement C3; C587883:HBEGF protein, human; D066257:Heparin-binding EGF-like Growth Factor; D036341:Intercellular Signaling Peptides and Proteins; D051916:Membrane Cofactor Protein; D012313:RNA; D003165:Complement System Proteins; D040281:Vascular Endothelial Growth Factor Receptor-1