Magic™ Anti-Retinol Binding Protein RBP (native) polyclonal antibody

Craniosynostosis is one of the most common congenital craniofacial deformities and could cause a series of diseases or defects. But the molecular mechanism underlying craniosynostosis is rarely reported. Retinal-binding protein 4 (RBP4) was shown to be involved in osteogenesis and decreased dramatically in prematurely fused suture. To investigate the role of RBP4 in osteogenesis, a cell line stably expressing RBP4 was constructed based on MC3T3-E1 cells and RBP4 overexpression was confirmed at both mRNA level and protein level. Then we found that RBP4 upregulation promoted proliferation of MC3T3-E1 cell and significantly increased alkaline phosphatase activity from day 7 to day 14 in MC3T3-E1 cells. Further, in alizarin red staining assay, RBP4 was shown to increase the deposit of calcium phosphate remarkably from day 14 to day 21 in MC3T3-E1 cells cultured in differentiated medium. This indicated that RBP4 prompted the mineralization of MC3T3-E1 cells. In accordance with this phenotype, we detected the typical osteo-differentiation markers by RT-qPCR and demonstrated that RUNX2, OC, OPN and COLL1 were greatly increased in RBP4-overexpressed MC3T3-E1 cells compared to the control. Therefore, our data suggest that RBP4 plays a positive role during osteogenesis and may be favorable for bone formation. This study provides us a new opinion about the role of RBP4 in craniosynostosis and RBP4 is worth of further study about its application on bone regeneration or bone development.

Cholesterol efflux capacity associates strongly and negatively with the incidence and prevalence of human CVD. We investigated the relationships of HDL's size and protein cargo with its cholesterol efflux capacity using APOB-depleted serum and HDLs isolated from five inbred mouse strains with different susceptibilities to atherosclerosis. Like humans, mouse HDL carried >70 proteins linked to lipid metabolism, the acute-phase response, proteinase inhibition, and the immune system. HDL's content of specific proteins strongly correlated with its size and cholesterol efflux capacity, suggesting that its protein cargo regulates its function. Cholesterol efflux capacity with macrophages strongly and positively correlated with retinol binding protein 4 (RBP4) and PLTP, but not APOA1. In contrast, ABCA1-specific cholesterol efflux correlated strongly with HDL's content of APOA1, APOC3, and APOD, but not RBP4 and PLTP. Unexpectedly, APOE had a strong negative correlation with ABCA1-specific cholesterol efflux capacity. Moreover, the ABCA1-specific cholesterol efflux capacity of HDL isolated from APOE-deficient mice was significantly greater than that of HDL from wild-type mice. Our observations demonstrate that the HDL-associated APOE regulates HDL's ABCA1-specific cholesterol efflux capacity. These findings may be clinically relevant because HDL's APOE content associates with CVD risk and ABCA1 deficiency promotes unregulated cholesterol accumulation in human macrophages.