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DOI 10.1016/j.cyto.2012.07.008

Медицинская библиотека · Cytokine · 2012

Umbilical artery chemokine CCL16 is associated with preterm preeclampsia and fetal growth restriction.

Mäkikallio Kaarin, Kaukola Tuula, Tuimala Jarno, F Kingsmore Stephen, Hallman Mikko, Ojaniemi Marja

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

BACKGROUND

Cytokines and growth factors synthesized by placental trophoblasts are suggested to induce endothelial and vascular smooth muscle cell apoptosis and affect angiogenesis.

OBJECTIVE

To investigate cord blood and placental immunoproteins in order to find new clues on pathogenetic factors of preterm preeclampsia.

METHODS

Cord blood samples were collected on 163 consecutive preterm deliveries prior to 32 gestational weeks. Placental function, clinical risk factors and 107 umbilical artery immunoproteins were analyzed. Classification and regression trees analysis was used to detect associations between the immunoproteins, clinical parameters and preterm preeclampsia. Placental expression of the immunoproteins and their receptors were subsequently investigated.

RESULTS

Preeclampsia complicated 34% of the pregnancies in this preterm cohort. Umbilical artery CCL16, CCL24, and CCL23 were associated with preeclampsia, CCL16 showing the strongest relationship with an OR (95% CI) of 24.5 (5.4-112.0). High umbilical artery CCL16 was also characteristic to fetuses with severe growth restriction (<3rd percentile). CCL16, CCL24 and their receptors, CCR1 and CCR3 were expressed in preeclamptic placentas.

CONCLUSIONS

High umbilical artery CCL16 is prominently detected in preterm preeclamptic pregnancies with severe growth restriction. A link to compensatory proangiogenic mechanisms has to be considered.

Для цитирования: Mäkikallio Kaarin, Kaukola Tuula, Tuimala Jarno, F Kingsmore Stephen, Hallman Mikko, Ojaniemi Marja. Umbilical artery chemokine CCL16 is associated with preterm preeclampsia and fetal growth restriction.. Cytokine. 2012. DOI: 10.1016/j.cyto.2012.07.008.

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