Abstract
As a member of the chemokine family, CXCL3 was previously known to participate in many pathophysiological events. However, whether CXCL3 stimulates trophoblast invasion as a key process of preeclampsia pathogenesis remains largely unknown. Therefore, the aim of this study was to investigate this hypothesis and determine the effect of CXCL3 on the first trimester trophoblast. Seventy gravidas were included in this study. ELISA was used to detect CXCL3 plasma levels on preeclampsia and normal pregnant groups. CXCL3 protein and mRNA levels were detected via Western blot and real-time quantitative PCR analysis after immunolocalized in human placenta. Moreover, the CXCL3 function in HTR-8/Svneo was analyzed via WST-1 assay, flow cytometry and invasion test. The plasma CXCL3 level in preeclampsia was significantly higher than that in normal pregnancy. CXCL3 expression was observed in the cytoplasm of placental trophoblasts and vascular endothelium in all groups without significant difference between maternal and fetal sides. In addition, placenta CXCL3 expression in severe preeclampsia was significantly lower than those in normal and mild PE groups. Moreover, exogenous CXCL3 can promote the proliferation and invasion of HTR-8/Svneo; however, its effect on apoptosis remains unclear. In summary, a significant abnormality of plasma CXCL3 level and placental CXCL3 expression was discovered in severe preeclampsia; CXCL3 had a function in trophoblast invasion, which indicated its participation in shallow implantation. Therefore CXCL3 might be involved in severe preeclampsia pathogenesis.
Highlights
Preeclampsia is an important and specific complication of pregnancy
The results showed that the plasma CXCL3 level of severe preeclampsia patients was positively correlated with 24 h urinary protein (r250.660) (Fig. 1B)
Umbilical artery chemokine CCL16 and CCL24 levels were significantly higher in preeclampsia cords [23]
Summary
Preeclampsia is an important and specific complication of pregnancy. This condition is characterized by the onset of hypertension after 20 weeks of gestation with accompanying proteinuria, which affects approximately 3.4% of all pregnancies [1]. Chemokines function as regulators of leukocyte migrate to damaged tissue site when inflammation or infection occurs. CXCL3 (GRO-c) belongs to the CXC family bearing(ELR+) motif, glutamic acid(E), leucine(L), and arginie(R). The ELR+ motif precedes the first two cysteines, which are separated by one amino acid (CXC) [6, 7]. CXCL3 functions after binding the receptor, CXCR2. CXCR2 promotes chemotaxis and angiogenesis via the extracellular signal-regulated protein kinase 1/2 (ERK 1/2) pathway after combining with ELR+ CXC chemokine. One recent study had demonstrated that CXCL3 is involved in precursors of cerebellar granule neuron migration [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
