Serum amyloid A-induced angiogenesis via scavenger receptor class B type 1 signaling pathway in rheumatoid arthritis / 中华风湿病学杂志

Objective To investigate the role of scavenger receptor class B type 1 (SR-B1) signaling pathway in serum amyloid A (SAA)-induced angiogenesis in rheumatoid arthritis (RA).Methods The expression and location of SR-B1 in RA and osteoarthritis (OA) synovial tissues were observed by immunohistochemistry.And SR-B1 expression in the resting human umbilical vein endothelial cells (HUVECs) was detected by immunoflourescence.Wound repair assessement and tube formation assessement were employed to evaluate the effect on cell migration and tube formation stimulated by SAA and/or anti-SR-B1 antibody.The t-test and one-way analysis of variance (ANOVA) were used for statistical analysis.Results ① SR-B1 was significantly highly expressed in RA tissue samples (A=6 788±819) when compared to the minimal expression in OA (A =31 849±6 977,t=3.567,P＜0.01).Positive staining of SR-B1 was observed in RA synovial vascular endothelial cells and perivascular areas.② Strong staining for SR-B1 was observed in all HUVECs tested.③ Significant wound healing induced by SAA (MI=2.50±0.17) was found compared with the untreated controls (MI=1.00±0.09,q=14.38,P＜0.01),and the effects were inhibited in the presence of anti-SR-B1 antibody (MI=1.16±0.14,q=13.02,P＜0.01).④ Compared to the untreated group (branch point number:6.6±0.8),there was an enhanced formation of branched and capillary-hke tube structure followed by SAA stimulation (branch point number:19.0±1.1,q=25.04,P＜0.01) after culturing for 72 h,whereas,tube formation decreased markedly upon pre-treated with anti-SR-B1 antibody (branch point number:7.6±1.3,vs SAA,q =23.32,P＜0.01).Conclusion Our present study suggests that serum amyloid A may induce angiogenesis via SR-B1 signaling pathway in RA.

Cholesterol ester transfer protein regulates the hepatic SR-B1 mRNA expression in mice / 中华内分泌代谢杂志

The effect of cholesterol ester transfer protein(CETP) on SR-B1 mRNA expression in mouse liver was investigated.The results demonstrated that CETP transgenic mice showed lower serum total cholesterol and high density lipoprotein-cholesterol levels but higher total cholesterol and cholesterol ester content in liver when compared with wild type mice(P＜0.05).The expression of SR-B1 mRNA in liver of CETP transgenic mice was significantly lower as compared with the control group(P＜0.05).

Lipopolysaccharide Down-regulates SR-BI Expression in a Nucleus Factor-κB Pathway-dependent Manner / 中国基层医药

Objective To investigate the changes of cholesterol efflux,the scavenger receptor class B type Ⅰ(SR-BI) protein expression in THP-1 maerophage derived foam cells treated with Lippolysaecharide (LPS), and to discover the role of NF-κB pathway in this process.Methods The foam cells were treated with LPS along or treated with N-p-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) for 24 h.The protein levels of SR-BI and intranuclear NF-κB p65 were measured by Western blotting.Cellular lipid accumulation was determined by high performance liquid ehromatograpby analysis.Cholesterol efflux was determined by FJ-2107P type liquid scintillator.Results The expression of SR-BI was decreased after treated with LPS,while the intranuclear NF-κB p65 protein level was increased by LPS.The results also showed that cellular lipid accumulation was increased ,while the cellular cholesterol efflux was decreased in THP-1 maerophage derived foam cells after exposed to LPS for 24 h and these changes can be reversed partly by pretreatment with TPCK.Conclusion LPS could down-regulate the expression of SR-BI, promote the accumulation of lipid and decrease cellular cholesterol efflux in THP-1 maerophage derived foam cells ,which should be related to the TLR4/NF-κB dependent pathway.

EFFECTS OF HIGH-FAT DIET ON LIPID METABOLISM IN SR-AⅠ/Ⅱ GENE KNOCK-OUT MICE / 营养学报

Objective To observe the alteration of scavenger receptor class A types Ⅰand Ⅱ (SR-AⅠ/Ⅱ) gene knock-out on lipid metabolism in mice fed with high-fat diet, and explore the underlying mechanism. Method The SR-AⅠ/Ⅱgene knock-out and wild-type male mice were fed with normal and high-fat diet for 12 w. Thereafter, the level of lipid metabolism (such as the levels of lipids in blood and liver) was detected with enzyme method or oil red O staining, and the expression of scavenger receptor class B typeⅠ(SR-BⅠ) and CD36 in liver was analyzed by RT-PCR. Results Under high-fat diet condition, as compared with wild-type mice, the levels of TG, TC, LDL and HDL in SR-AⅠ/Ⅱgene knock-out mice were decreased at 3, 6, 12 w (P0.05). Conclusion The alteration of lipid metabolism induced by high-fat diet in SR-AⅠ/Ⅱgene knock-out mice might be relative with the up-regulated SR-BⅠmRNA expression and the counter transport of peripheral lipids to liver.