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Electron Microscopical Localisation of CD61 (Beta3 Integrin) on Placental Syncytiotrophoblast Microvilli
Author(s) -
Kumpel B.,
Jackson D.,
Sibley K.,
White G.
Publication year - 2006
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1111/j.1365-3148.2006.00694_53.x
Subject(s) - syncytiotrophoblast , neonatal alloimmune thrombocytopenia , staining , uranyl acetate , brush border , placenta , andrology , fetus , chemistry , biology , pathology , pregnancy , medicine , vesicle , biochemistry , genetics , membrane
Neonatal alloimmune thrombocytopenia (NAIT) due to maternal antibodies to the human platelet antigen (HPA)‐1a can occur in first pregnancies. The HPA‐1 polymorphism is located on platelet glycoprotein (GP)IIIa (CD61, beta3 integrin). It is hypothesised that besides fetal platelets, an additional source of fetal CD61 could cause alloimmunisation early in pregnancy. CD61 was earlier identified on placental villous trophoblasts by immunocytochemistry. Methods Whole‐mount immuno‐electron microscopy was used to study the ultrastructural localisation of CD61 on placental tissue. Fragments of first trimester ( n = 5, 8–12 weeks gestational age) and term ( n = 1) placental chorionic villi were incubated with anti‐CD61 or IgG1 isotype control, washed, incubated with 18 nm colloidal gold‐conjugated anti‐mouse IgG, washed, fixed in phosphate‐buffered glutaraldehyde and processed through to embedding in epoxy resin. 100 nm sections were prepared from the EM blocks; these were stained with uranyl acetate and lead citrate, and examined with a Phillips CM10 electron microscope. Positive control was term tissue stained with anti‐placental alkaline phosphatase (PLAP). Results Microvilli were observed on the apical membrane of some but not all of the villous syncytiotrophoblast (STB) surfaces. Formation of this brush border occurs during the first trimester to increase the surface area of these cells for optimal transfer of nutrients and gases from the adjacent maternal blood to the fetus. All specimens had some microvilli. After staining with anti‐CD61, gold particles were present on and between some microvilli of all specimens, either singly or in small groups. Stronger staining with more frequent occurrence of groups of gold particles was evident on microvilli of the term tissue incubated with anti‐PLAP. No gold particles were seen on the isotype control specimens. Conclusion From early on in pregnancy, CD61 is present on the surface of fetal STB in contact with maternal blood. This protein carrying the HPA‐1 polymorphism might be the cause of the initial immunising event that leads to NAIT.