Decreased expression of MMP-9 in CD8+ cells in placenta with severe preeclampsia.

We compared the number of CD4-positive (CD4+) and CD8-positive (CD8+) cells in severe and non-severe preeclampsia (PE), and in normal pregnancy. We also evaluated the expression of matrix metalloproteinase 9 (MMP-9) in CD4+ and CD8+ cells. Immunohistochemistry for CD4+ and CD8+ was performed on the decidua basalis of 15 severe and 13 non-severe PE women and compared to decidual tissue of 19 normal pregnancies (control group). Co-expression of MMP-9 with CD8+ and CD4+ cells was determined by double immunofluorescence staining. The median number of CD8+ cells/mm2 was significantly lower for the severe PE group than for the normal pregnancy group, as was the number of CD4+ cells and MMP-9+CD8+ cells. No statistical difference was found between the non-severe PE group and the normal pregnancy group. The significant decrease of CD4+, CD8+ and MMP-9+CD8+ cells at the fetal-maternal interface only in the severe PE group suggests that immunological disorders play a role in the pathophysiology of severe PE.

Expression of cytokeratin 8, vimentin, syndecan-1 and Ki-67 during human tooth development.

Spatio-temporal immunolocalizations of cytokeratin 8 (CK8), vimentin, syndecan-1 and Ki-67 were analyzed in ten human incisors and canine tooth germs between the 7th and 20th developmental weeks. CK8 expression was mild to moderate in the epithelial tooth parts, while it shifted from absent or mild in its mesenchymal parts, but few cells, sparsely distributed throughout the tooth germ, strongly expressed CK8. As development progressed, CK8 expression increased to strong in preameloblasts, while expression of vimentin increased to moderate in the epithelial and mesenchymal tooth parts, particularly in the dental papilla and sac. Co-expression of CK8 and vimentin was observed in some parts of the tooth germ, and was increasing in the differentiating preameloblasts and preodontoblasts. Syndecan-1 showed characteristic shift of expression from epithelial to mesenchymal tooth parts, being particularly strong in dental papilla, sac and cervical loops, while co-expression of Ki-67/syndecan-1 was strong in the dental papilla. Our study demonstrated spatio-temporal expression and restricted co-expression of the investigated markers, indicating participation of CK8 and vimentin in cell proliferation and migration, and differentiation of preodontoblasts and preameloblasts. Our data also suggest involvement of syndecan-1 in morphogenesis of the developing tooth crown and cervical loops, and together with CK8 and vimentin in differentiation of preameloblasts and preodontoblasts.

The involvement of proliferation and apoptosis in the early human gonad development.

Distributions of the Ki-67, TP53, caspase-3 and AIFM1 markers were histologically investigated in the 5th to 9th week developing gonads of 12 human conceptuses using immunohistochemical and immunofluorescence methods. Between the 5th and 8th developmental week, proliferation gradually increased in the surface gonad epithelium (26-52 %) and stroma (19-42 %), but then slightly decreased in the surface epithelium (35 %) during the early foetal period. In medulla, low proliferation activity decreased from 15 to 12 % between the 7th and 9th week. At earliest stages of gonadal development, primordial germ cells (PGC) were only rarely TP53 positive. In the 7th and 8th week, almost all PGC-s displayed TP53 positivity, while their number decreased in early fetal period. During the investigated period, caspase-3 reactivity gradually decreased in surface epithelium, while it increased in PGC and medulla of developing gonad AIFM1-positivity first appeared in surface gonad epithelium and then predominantly in PCG-s while caspase-3 characterized different cell populations within the developing gonad. AIFM1 and caspase-3 co-localized only during the migration of PCG-s. The number and distribution of Ki-67, TP53, caspase-3 and AIFM1 reacting cells changed coincidently with development end regression of the sex cords in indifferent and early fetal gonad. Our results indicate that the number of PGC might be controlled by balance of TP53 and AIFM1, leading to caspase-3 independent cell death. Other cell populations are probably eliminated by caspase-3-dependent cell death. Both pathways of cell death seem to operate during early human gonad development, while their intensity varies depending on the cell type and developmental period analysed.