Inconformity of CXCL3 Plasma Level and Placenta Expression in Preeclampsia and Its Effect on Trophoblast Viability and Invasion

<div><p>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.</p></div

Clinical characteristics of study participants.

<p>Data are presented as mean ± standard error of the mean.</p><p>☆:Full term pregnancy compared with preterm pregnancy in mild PE group, P<0.05;</p><p>△:Severe PE group compared with normal pregnant group, P<0.05;</p><p>▴:Severe PE group compared with mild PE group, P<0.05.</p><p>Clinical characteristics of study participants.</p

Plasma CXCL3 concentration.

<p>A:Plasma CXCL3 levels of normal pregnant women, mild preeclamptic pregnant women and severe preeclamptic pregnant women. Middle line: median; Whisker: standard deviation. B: The correlation between plasma CXCL3 levels of the severe PE group participants with 24-hour urinary protein.</p

Effect of rhCXCL3 on the viability of trophoblast cells.

<p>Bar: mean; Whisker: standard deviation. A: HTR-8/SVneo cell viability in different rhCXCL3 concentration. B: Cell viability at different time intervals (12, 24, 48, and 72 h) . a: p<0.05, versus 12 h; b: p<0.05, versus 24 h. C: Cell viability in different rhCXCL3 concentration. a: a: p<0.05, versus 0 ng/ml; b: p<0.05, versus 1 ng/ml; c: p<0.05, versus 10 ng/ml; d: p<0.05, versus 50 ng/ml.</p

Additional file 1: of Higher serum 25(OH)D level is associated with decreased risk of impairment of glucose homeostasis: data from Southwest China

Table S1. The diagnosis of pre-diabetes (n = 1514). (DOCX 16 kb

Additional file 2: of Higher serum 25(OH)D level is associated with decreased risk of impairment of glucose homeostasis: data from Southwest China

Table S2. Multiple logistic regression odds ratio (OR) and 95% confidence interval (CI) for the association of tertiles of serum 25(OH)D (ng/ml) with pre-diabetes1 (DOCX 18 kb

A: Invasion trophoblast cells stained by eosin under microscope (×400).

<p>A: 0 ng/ml rhCXCL3; B: 1 ng/ml rhCXCL3; C: 10 ng/ml rhCXCL3; D: 50 ng/ml rhCXCL3; E: 100 ng/ml rhCXCL3; F: 200 ng/ml rhCXCL3. G: Effect of rhCXCL3 on the invasiveness of trophoblast cells. Bar: mean; Whisker: standard deviation. a: p<0.05, versus 0 ng/ml; b: p<0.05, versus 1 ng/ml.</p

CXCL3 expression in placentae of three groups (Immunohistochemistry, SP, ×400).

<p>(S: syncytiotrophoblast; V: vascular endothelial cells) A: CXCL3 expressed on maternal surface of normal placentae; B: CXCL3 expressed on maternal surface of mild preeclamptic placentae; C: CXCL3 expressed on maternal surface of severe preeclamptic placentae; D: CXCL3 expressed on fetal surface of normal placentae; E: CXCL3 expressed on fetal surface of mild preeclamptic placentae; F: CXCL3 expressed on fetal surface of severe preeclamptic placentae; G: negative control; H: human colon adenocarcinoma tissue as positive control.</p

Stabilizing Nanostructured Solid Oxide Fuel Cell Cathode with Atomic Layer Deposition

We demonstrate that the highly active but unstable nanostructured intermediate-temperature solid oxide fuel cell cathode, La_0.6Sr_0.4CoO_3‑δ (LSCo), can retain its high oxygen reduction reaction (ORR) activity with exceptional stability for 4000 h at 700 °C by overcoating its surfaces with a conformal layer of nanoscale ZrO₂ films through atomic layer deposition (ALD). The benefits from the presence of the nanoscale ALD-ZrO₂ overcoats are remarkable: a factor of 19 and 18 reduction in polarization area-specific resistance and degradation rate over the pristine sample, respectively. The unique multifunctionality of the ALD-derived nanoscaled ZrO₂ overcoats, that is, possessing porosity for O₂ access to LSCo, conducting both electrons and oxide-ions, confining thermal growth of LSCo nanoparticles, and suppressing surface Sr-segregation is deemed the key enabler for the observed stable and active nanostructured cathode