Objective To observe the effect of acetylated low-density lipoprotein (AcLDL) on the expression of adipophilin and the effect of adipophilin on AcLDL uptake and lipid accumulation in human vascular smooth muscle cells (HVSMCs)in order to approach the role played by adipophilin in genesis of macroangiopathy. Methodse HVSMCs were treated with various amount of AcLDL. Adipophilin expression levels were detected by Northern blot and Western blot. The effects of adipophilin on AcLDL uptake and lipid accumulation in HVSMCs were observed by the methods of siRNA, flow cytometry, enzymatic method and oil red stain. Results AcLDL dose-dependently increased adipophilin expression in HVSMCs. Silence adipophilin by siRNA decreased AcLDL uptake (decreasing by 38.7%, P<0. 05) and lipids accumulation (tfiglyceride and total cholesterol decreasing by 30.6% and 29.8% respectively, both P<0. 01) in HVSMCs, Conclusion Adipophilin is able to increase AcLDL uptake and lipid accumulation in HVSMCs, suggesting that it might play a role in enhancing atherosclerosis.

AIM:To study the effect of astragalus polysaccharides(Aps)on cholesterol efflux in THP-1 macrophage-derived foam cells.METHODS:After exposed to Aps at different doses,cholesterol efflux and ABCA1 protein levels in cultured THP-1 macrophage-derived foam cells were determined by a ? counter and flow cytometry,respectively.RESULTS:Aps increased cholesterol efflux in THP-1 macrophage-derived foam cells with dose dependent pattern and resulted in an increase in the expression of ABCA1 protein in THP-1 macrophage-derived foam cells.CONCLUSION:The increase in cholesterol efflux by Aps might be related to the up-regulation of ABCA1.

The mechanisms underlying pregnancy complications caused by advanced maternal age(AMA)remain unclear.We analyzed the cellular signature and transcriptomes of human placentas in AMA women to elucidate these mechanisms.Placental tissues from two AMA women and two controls were used for single-cell RNA-sequencing(scRNA-seq).Controls consisted of AMA women who did not experience any pregnancy complications and pregnant women below the age of 35 years without pregnancy complications.Trophoblast cells were obtained from the placentas of another six pregnant women(three AMA women and three controls),and in-vitro transwell assays were conducted to observe the cell invasion ability.Thirty additional samples(from 15 AMA women and 15 controls)were analyzed to verify the specific expression of serine protease inhibitor clade E member 1(SERPINE1).Preliminary study of the role of SERPINE1 in cell invasion was carried out with HTR8-S/Vneo cells.High-quality transcriptomes of 27 607 cells were detected.Three types of trophoblast cells were detected,which were further classified into eight subtypes according to differences in gene expression and Gene Ontology(GO)function.We identified 110 differentially expressed genes(DEGs)in trophoblast cells between the AMA and control groups,and the DEGs were enriched in multiple pathways related to cell invasion.In-vitro transwell assays suggested that the invading trophoblast cells in AMA women were reduced.SERPINE1 was specifically expressed in the trophoblast,and its expression was higher in AMA women(P＜0.05).Transfection of human SERPINEl(hSERPINE1)into HTR8-S/Vneo trophoblast cells showed fewer invading cells in the hSERPINE1 group.Impaired cell invasion may underlie the increased risk of adverse pregnancy outcomes in AMA women.Abnormal expression of SERPINE1 in extravillous trophoblast(EVT)cells appears to play an important role.