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| 3. |
- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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| 4. |
- Niemi, MEK, et al.
(författare)
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- 2021
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| 5. |
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| 6. |
- Tabiri, S, et al.
(författare)
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- 2021
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| 7. |
- Kanai, M, et al.
(författare)
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- 2023
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| 8. |
- Tornblom, SA, et al.
(författare)
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15-Hydroxyprostaglandin dehydrogenase and cyclooxygenase 2 messenger ribonucleic acid expression and immunohistochemical localization in human cervical tissue during term and preterm labor
- 2004
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 1945-7197 .- 0021-972X. ; 89:6, s. 2909-2915
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Tidskriftsartikel (refereegranskat)abstract
- Here we have examined the enzymes cyclooxygenase (COX)-2 and 15-hydroxyprostaglandin dehydrogenase (15-OH PGDH) in pregnant human cervix. In biopsies taken transvaginally after preterm and term elective cesarean sections and vaginal deliveries, the levels of mRNA coding for COX-2 and 15-OH PGDH were assessed by Northern blotting. The cellular localization of the COX-2 and 15-OH PGDH proteins was determined by immunohistochemical analysis. COX-2 and 15-OH PGDH mRNAs were expressed at detectable levels in the cervical biopsies from all four groups of subjects. At cesarean sections ( unripe cervix), the level of 15-OH PGDH mRNA was significantly higher than the level in the ripe cervix at the time of partus, irrespective of the gestational length. In contrast, the level of COX-2 mRNA was similar in all subjects. Immunoreactivity of COX-2 and 15-OH PGDH was expressed by activated fibroblasts. The present investigation documents the expression and cellular localization of COX-2 and 15-OH PGDH in the preterm and term pregnant human cervix. This observation indicates that both preterm and term cervical ripening is associated with decreased degradation of prostaglandins.
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| 9. |
- Yougbare, I, et al.
(författare)
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Activated NK cells cause placental dysfunction and miscarriages in fetal alloimmune thrombocytopenia
- 2017
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Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 8:1, s. 224-
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Tidskriftsartikel (refereegranskat)abstract
- Miscarriage and intrauterine growth restriction (IUGR) are devastating complications in fetal/neonatal alloimmune thrombocytopenia (FNAIT). We previously reported the mechanisms for bleeding diatheses, but it is unknown whether placental, decidual immune cells or other abnormalities at the maternal–fetal interface contribute to FNAIT. Here we show that maternal immune responses to fetal platelet antigens cause miscarriage and IUGR that are associated with vascular and immune pathologies in murine FNAIT models. Uterine natural killer (uNK) cell recruitment and survival beyond mid-gestation lead to elevated NKp46 and CD107 expression, perforin release and trophoblast apoptosis. Depletion of NK cells restores normal spiral artery remodeling and placental function, prevents miscarriage, and rescues hemorrhage in neonates. Blockade of NK activation receptors (NKp46, FcɣRIIIa) also rescues pregnancy loss. These findings shed light on uNK antibody-dependent cell-mediated cytotoxicity of invasive trophoblasts as a pathological mechanism in FNAIT, and suggest that anti-NK cell therapies may prevent immune-mediated pregnancy loss and ameliorate FNAIT.
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| 10. |
- Glasbey, JC, et al.
(författare)
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- 2021
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