Only in Titles

Search results for: ABCA1 Antibody

paperclip

#33741356   2021/03/16 To Up

The ABCA1-efferocytosis axis: A new strategy to protect against atherosclerosis.

Atherosclerosis, a disease process characterized by lipid accumulation and inflammation, is the main cause of coronary heart disease (CHD) and myocardial infarction (MI). Efferocytosis involves the clearance of apoptotic cells by phagocytes. Successful engulfment triggers the release of anti-inflammatory cytokines to suppress atherosclerosis. ABCA1 is a key mediator of cholesterol efflux to apoA-I for the generation of HDL-C in reverse cholesterol transport (RCT). Intriguingly, ABCA1 promotes not only cholesterol efflux but also efferocytosis. ABCA1 promotes efferocytosis by regulating the release of "find-me" ligands, including LPC, and the exposure, release, and expression of "eat-me" ligands, including PtdSer, ANXA1, ANXA5, MEGF10, and GULP1. ABCA1 has a pathway similar to TG2, which is an "eat-me" ligand. ABCA1 has the highest known homology to ABCA7, which controls efferocytosis as the engulfment and processing ligand. In addition, ABCA1 can form several regulatory feedback axes with ANXA1, MEGF10, GULP1, TNFα, and IL-6. Therefore, ABCA1 is the central factor that links cholesterol efflux and apoptotic cell clearance. Several drugs have been studied or approved for apoptotic cell clearance, such as CD47 antibody and PD1-/PD-L1 antibody. In this article, we review the role and mechanism of action of ABCA1 in efferocytosis and focus on new insights into the ABCA1-efferocytosis axis and its potential as a novel therapeutic target in atherosclerosis.
Wujun Chen, Lu Li, Jie Wang, Renshuai Zhang, Tingting Zhang, Yudong Wu, Shuai Wang, Dongming Xing

2329 related Products with: The ABCA1-efferocytosis axis: A new strategy to protect against atherosclerosis.

2.5 mg1 ml1 mL1 module5 mg1 kit(96 Wells)

Related Pathways

paperclip

Error loading info... Pleas try again later.
paperclip

#32782494   2020/06/19 To Up

Curcumin affects ox-LDL-induced IL-6, TNF-α, MCP-1 secretion and cholesterol efflux in THP-1 cells by suppressing the TLR4/NF-κB/miR33a signaling pathway.

The aim of the present study was to study the molecular mechanism of how curcumin decreases the formation of ox-LDL induced human monocyte macrophage foam cells, promotes the efflux of cholesterol and reduces the secretion of inflammatory cytokines. cultured THP-1 cells were induced to become macrophages using phorbol-12-myristate-13-acetate. The cells were then pre-treated with curcumin before inducing the foam cell model by addition of oxidized low-density lipoprotein (ox-LDL). Western blot assays were used to detect expression levels of toll-like receptor (TLR)4, nuclear factor κB (NF-κB), NF-κB inhibitor α (IκBα), phosphorylated-IκBα and ATP binding cassette transporter (ABC)A1. Reverse transcription-quantitative PCR was employed to examine mRNA levels of TLR4, microRNA (miR)33a and ABCA1. ELISAs were used to detect inflammatory factors, including tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1 and interleukin (IL)-6. ox-LDL successfully induced the foam cell model, promoted phosphorylation of IκBα, promoted nuclear translocation of NF-κB, promoted the expression of TLR4 and miR33a, and promoted the secretion of TNF-α, MCP-1 and Il-6. Additionally, ox-LDL reduced the expression of ABCA1 and cholesterol efflux. However, pretreatment with curcumin increased the expression of ABCA1 and cholesterol efflux and suppressed secretion of TNF-α, MCP-1 and Il-6. TLR4 antibodies, the NF-κB blocker, PDTC, and the miR33a inhibitor also reduced the abnormal transformations induced by ox-LDL. Curcumin promoted cholesterol efflux by suppressing the TLR4/NF-κB/miR33a signaling pathway, and reduced the formation of foam cells and the secretion of inflammatory factors.
Yi Zhong, Cheng Liu, Jian Feng, Jia-Fu Li, Zhong-Cai Fan

2282 related Products with: Curcumin affects ox-LDL-induced IL-6, TNF-α, MCP-1 secretion and cholesterol efflux in THP-1 cells by suppressing the TLR4/NF-κB/miR33a signaling pathway.

1x10e7 cells1x10e7 cells1x10e7 cells1x10e7 cells100ug1x10e7 cells 100ul100ug25 mg100ug2 Pieces/Box100ul

Related Pathways

paperclip

Error loading info... Pleas try again later.
paperclip

#32113776   2020/02/26 To Up

Novel milk casein-derived peptides decrease cholesterol micellar solubility and cholesterol intestinal absorption in Caco-2 cells.

This study sought to assess the cholesterol-lowering activity of peptides obtained from milk casein hydrolyzed with neutrase. The bioactive peptides were separated using a Sephadex G-10 chromatographic column (Amersham Pharmacia Biotech, Uppsala, Sweden) after ultrafiltration using a 1-kDa molecular mass cutoff membrane. Via ultra-performance liquid chromatography-electrospray ionization-tandem mass spectrometry, we determined that peptides Thr-Asp-Val-Glu-Asn [TDVEN; β-casein f(143-147)], Leu-Gln-Pro-Glu [LQPE; β-casein f(103-106)], Val-Ala-Pro-Phe-Pro-Glu [VAPFPE; α-casein f(40-45)], and Val-Leu-Pro-Val-Pro-Gln [VLPVPQ β-casein f(185-190)] reduced micellar cholesterol solubility. After Caco-2 cells were treated with LQPE, VLPVPQ, and VAPFPE, the Niemann-Pick C1-Like 1 (NPC1L1) protein levels decreased by (means ± SEM) 19.33 ± 2.47%, 52.1 ± 3.77%, and 23.09 ± 8.52%, respectively, compared with the control group. Treatment with each peptide induced significant upregulation of ATP binding cassette subfamily G member 8 antibody (ABCG8) mRNA expression by 398.1 ± 23.27%, 86.4 ± 27.07%, and 92.8 ± 8.49%. We found that VLPVPQ and LQPE significantly upregulated ATP-binding cassette transporter A1 (ABCA1) transcription by 203.9 ± 8.44% and 220.8 ± 36.42% respectively, whereas VLPVPQ significantly decreased mRNA expression of acetyl-CoA-acetyltransferase 2 (ACAT2) and microsomal triacylglycerols (MTP). The cholesterol-lowering action of milk-derived peptides may be induced by suppression of micellar cholesterol solubility and affects the expression of cholesterol absorption-related proteins and enzymes in intestinal epithelial cells. This research discovers new milk-derived peptides with decreasing cholesterol micellar solubility and provides a theoretical basis of in vitro cholesterol-lowering effects of peptides.
Xiaoxiao Jiang, Daodong Pan, Tao Zhang, Chen Liu, Jiaxin Zhang, Mi Su, Zhen Wu, Xiaoqun Zeng, Yangying Sun, Yuxing Guo

1094 related Products with: Novel milk casein-derived peptides decrease cholesterol micellar solubility and cholesterol intestinal absorption in Caco-2 cells.

96 wells96 wells96 assays5 x 200ul/Unit2000 pcs200ul250ul100ug Lyophilized1.00 flask20ug50 mg

Related Pathways

paperclip

#31970862   2020/01/22 To Up

Inhibition of USP14 suppresses the formation of foam cell by promoting CD36 degradation.

Atherosclerosis is regarded as a chronic progressive inflammatory disease and is a basic pathophysiological process in coronary artery disease which is life threatening in clinic. The formation of foam cell plays a key role in the pathogenesis of atherosclerosis. OxLDL is a significant factor in progression of coronary artery disease. Our studies have demonstrated that USP14 promotes cancer development and mediates progression of cardiac hypertrophy and LPS-induced inflammation. However, the underlying mechanism of USP14 is unknown. In this study, we found that the inhibition of USP14 significantly suppressed the oxLDL uptake, subsequently decreased the foam cell formation. Surprisingly, USP14 has an effect on the expression of CD36 but not SR-A, ABCA1, Lox-1, ABCG1 and SR-Bl. Furthermore, USP14 stabilizes CD36 protein via cleaving the ubiquitin chain on CD36. Blocking CD36 activation using antibody-dependent blocking assay remarkably attenuated the function of USP14 on the formation of foam cell. In summary, our results suggested that the inhibition of USP14 decreases foam cell formation by down-regulating CD36-mediated lipid uptake and provides a potential therapeutic target for atherosclerosis.
Fangcheng Zhang, Xiaohong Xia, Renjie Chai, Ruqin Xu, Qiong Xu, Mingke Liu, Xuke Chen, Bin Liu, Shiming Liu, Ningning Liu

2271 related Products with: Inhibition of USP14 suppresses the formation of foam cell by promoting CD36 degradation.

5 G10 ml1.5 x 10^6 cells30 isolations1.00 flask500 ml100 ml100 ug

Related Pathways

paperclip

Error loading info... Pleas try again later.
paperclip

#31654747   2019/10/22 To Up

Effects of β2/aβ2 on oxLDL-induced CD36 activation in THP-1 macrophages.

β2-glycoprotein I/anti-β2-glycoprotein I antibody complex (β2/aβ2) could promote oxLDL-induced endothelial inflammation through Toll-like receptor 4 (TLR4), therefore accelerates atherosclerosis in patients with anti-phospholipid syndrome (APS). However, effects of β2/aβ2 and TLR4 on oxLDL-induced CD36 activation in macrophages remain to be elucidated and are currently under investigation.
Chao He, Guiting Zhang, Hang Ouyang, Peng Zhang, Yudan Chen, Ren Wang, Hong Zhou

2313 related Products with: Effects of β2/aβ2 on oxLDL-induced CD36 activation in THP-1 macrophages.

100ug100ug100μg 100ul100μg100ug10 mg100ug Lyophilized10ug100ug Lyophilized1 g1000

Related Pathways

paperclip

#31443207   2019/08/15 To Up

Relationship between HDL Cholesterol Efflux Capacity, Calcium Coronary Artery Content, and Antibodies against ApolipoproteinA-1 in Obese and Healthy Subjects.

To explore the associations between cholesterol efflux capacity (CEC), coronary artery calcium (CAC) score, Framingham risk score (FRS), and antibodies against apolipoproteinA-1 (anti-apoA-1 IgG) in healthy and obese subjects (OS).
Nicolas Vuilleumier, Sabrina Pagano, Fabrizio Montecucco, Alessandra Quercioli, Thomas H Schindler, François Mach, Eleonora Cipollari, Nicoletta Ronda, Elda Favari

1023 related Products with: Relationship between HDL Cholesterol Efflux Capacity, Calcium Coronary Artery Content, and Antibodies against ApolipoproteinA-1 in Obese and Healthy Subjects.

1000 TESTS/0.65ml100ul100ug10 mg1000 tests100 mg100ug100ul100ug25 mg100ug2.5 mg

Related Pathways

paperclip

#31336517   2019/03/08 To Up

ABCA1 and metabolic syndrome; a review of the ABCA1 role in HDL-VLDL production, insulin-glucose homeostasis, inflammation and obesity.

ATP-binding cassette transporter A1 (ABCA1) is an integral cell-membrane protein that mediates the rate-limiting step of high density lipoprotein (HDL) biogenesis and suppression of inflammation by triggering a number of signaling pathways via interacting with an apolipoprotein acceptor. The hepatic ABCA1 is involved in regulation of very low density lipoprotein (VLDL) production by affecting the apolipoprotein B trafficking and lipidation of VLDL particles. This protein is involved in protecting the function of pancreatic β-cells and insulin secretion by cholesterol homeostasis. Adipose tissue lipolysis is associated with ABCA1 activity. This transporter is involved in controlling obesity and insulin sensitivity by regulating triglyceride (TG) lipolysis and influencing on adiponectin, visfatin, leptin, and GLUT4 genes expression. The ABCA1 of skeletal muscle cells play a role in increasing the glucose uptake by enhancing the Akt phosphorylation and transferring GLUT4 to the plasma membrane. Abnormal status of ABCA1-regulated phenotypes is observed in metabolic syndrome. This syndrome is associated with the occurrence of many diseases. This review is a summary of the role of ABCA1 in HDL and VLDL production, homeostasis of insulin and glucose, suppression of inflammation and obesity controlling to provide a better insight into the association of this protein with metabolic syndrome.
Mohammad Mahdi Babashamsi, Saeideh Zamani Koukhaloo, Sohrab Halalkhor, Ali Salimi, Mohammad Babashamsi

1535 related Products with: ABCA1 and metabolic syndrome; a review of the ABCA1 role in HDL-VLDL production, insulin-glucose homeostasis, inflammation and obesity.

2 Pieces/Box100 μg96 assays8 Sample Kit100ug100ul100ug200ul100ug100ug100ug100ug Lyophilized

Related Pathways