Human RBP4(Retinol-binding protein 4) ELISA Kit

Objective: Preeclampsia (PE) is a disorder of pregnancy that is associated with maternal and fetal mortality and morbidity. Abnormal placental Retinol-binding protein 4 (RBP4) expression has been found in cases of PE. This study aimed to further investigate the possible role of RBP4 in the pathophysiology of PE. Study Design: RBP4 serum concentration was detected using enzyme-linked immunosorbent assays in eighteen patients with severe PE and twenty-five individuals with healthy pregnancies. JEG-3 cells were transiently transfected with a plasmid construct expressing RBP4 (pCMV-RBP4), an empty plasmid (p-CMV) or siRNA, and the MMP2 and MMP9 protein levels were analysed 48 h after transfection. MTT assays and transwell assays were used to explore the functional role of RBP4 in the proliferation and invasion of JEG-3 cells. Results: RBP4 serum concentration in patients with severe PE was significantly lower than that in individuals with healthy pregnancies. RBP4 over-expression enhanced the invasion and proliferation of JEG-3 cells and increased MMP2 and MMP9 in JEG-3 cells. Conclusions: RBP4 plays an important role in the regulation of trophoblast invasion and migration and represents a possible underlying pathological and molecular mechanism of PE.

Retinol-binding protein 4 (RBP4) is a newly discovered adipocytokine related to insulin resistance (IR). Hyperinsulinemia and IR are the major risk factors for cardiovascular diseases (CVD). The role of RBP4 in CVD has not yet been determined. The present study was designed to analyze the correlation of RBP4 and CVD risk factors and to evaluate the role of RBP4 in proliferation of vascular smooth muscle cells during hyperinsulinemia and the underlying mechanisms. Plasma RBP4 concentration, IR-related indexes, and cardiovascular risk factors were measured from blood samples of hyperinsulinemic rats (HIns) and control SD rats (Cons). The vascular morphology and the expression of ERK1/2, p-ERK1/2 in arterial tissues of rats were assessed. Different concentrations of RBP4 (1, 4 mu g/ml) were used as intervention factor during insulin-induced aortic smooth muscle cells (RAS-MCs) proliferation. The expression of cell growth signaling pathways was assessed to identify the active pathway during this proliferation. Specifically, ERK1/2 inhibitor PD98059 and JAK2 inhibitor AG490 were used to detect it. RBP4 expression was higher in HIns compared with Cons p < 0.01). Plasma RBP4 concentrations were positively correlated with TG (r = 0.490), hsCRP (r = 0.565), media thickness (r = 0.890), and p-ERK1/2 protein (r = 0.746) (p < 0.05 each). In cultured RASMCs, RBP4 enhanced insulin-induced proliferation of cells and expression of p-ERK1/2 and p-JAK2. Blockade of ERK1/2 signaling pathway inhibited RBP4-induced proliferation of RASMCs, while suppressing JAK2 remains unchanged. These results suggest that plasma RBP4 concentrations were associated with CVD. In addition, RBP4 increases the proliferation of VSMCs induced by hyperinsulinism via activation of MAPK signaling pathway.