TY - JOUR
T1 - Pre-eclampsia affects procalcitonin production in placental tissue
AU - Agostinis, Chiara
AU - Rami, Damiano
AU - Zacchi, Paola
AU - Bossi, Fleur
AU - Stampalija, Tamara
AU - Mangogna, Alessandro
AU - Amadio, Leonardo
AU - Vidergar, Romana
AU - Vecchi Brumatti, Liza
AU - Ricci, Giuseppe
AU - Celeghini, Claudio
AU - Radillo, Oriano
AU - Sargent, Ian
AU - Bulla, Roberta
PY - 2018/4/1
Y1 - 2018/4/1
N2 - Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.
AB - Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.
KW - adalimumab
KW - calcitonin gene-related peptide
KW - placenta
KW - pre-eclampsia
KW - procalcitonin
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U2 - 10.1111/aji.12823
DO - 10.1111/aji.12823
M3 - Article
C2 - 29427369
AN - SCOPUS:85041740708
SN - 1046-7408
VL - 79
JO - Early pregnancy (Online)
JF - Early pregnancy (Online)
IS - 4
M1 - e12823
ER -