Apolipoprotein M (APOM) ELISA Kits

Human Apolipoprotein M (APOM) interaction partners

1. Plasma APOM levels were reduced in patients with chronic kidney disease stages 3-5D and this was mainly due to differences in plasma HDL-cholesterol.

2. \the results demonstrate that apoM-S1P inhibits ox-LDL-induced inflammation in HUVECs via the S1PR2-mediated PI3K/Akt signaling pathway.

3. Study shows that high-density lipoproteins (HDL) promotes increased export of sphingosine-1-phosphate (S1P) from human erythrocytes and that this is further enhanced by the presence of apoM. Also, apoM induces S1P export from erythrocytes independently of binding to HDL particles.

4. he results demonstrated that CDCA and apoM may modulate TF isoforms in different cell lines, and suggested that asTF may serve a role in the pathophysiological mechanism underlying cervical cancer development. In conclusion, the TF isoforms serve important and distinct roles in pathophysiological processes

5. These results suggested that PPARgamma regulates the S1P levels by modulating apoM in a bell-shaped manner, with the greatest levels of apoM/S1P observed when PPARgamma was mildly expressed and that hepatic apoM/PPARgamma axis might maintain the homeostasis of S1P metabolism.

6. apoM could be bound to high-density lipoprotein after secretion and then quickly exchanged with a non-lipoprotein-related compartment and to LDL to be slowly catabolized.

7. Obese patients showed significantly lower plasmatic ApoM levels than people with normal body weight, and ApoM level showed a strong correlation with CRP, TNF-alpha, and IL-6 levels, which indicated that ApoM might be regulated by these inflammatory factors.

8. These results demonstrated that ApoM protein mass were clearly higher in the NSCLC tissues than in non-small cell lung cancer (NSCLC) tissues. Overexpression of ApoM could promote NSCLC cell proliferation and invasion in vitro and tumor growth in vivo, which might be via upregulating S1PR1 and activating the ERK1/2 and PI3K/AKT signaling pathways.

9. results do not suggest a diagnostic role for ApoM plasma levels in patients with primary VTE. Moreover, the current study suggests that role of ApoM as a risk factor may differ for primary VTE and recurrent VTE in male patients.

10. These S1P-induced enhancements in growth factors and chemotactic cytokines in retinal pigment epithelium cells were significantly inhibited by ApoM treatment. Additionally, in vivo experiments using a laser-induced choroidal neovascularization (CNV) murine model demonstrated that intravitreal ApoM injection significantly reduced the progression of CNV formation.

11. The potential of mean force for sphingosine-1-phosphate unbinding from apoM reflected a large binding strength of more than 60 kJ/mol. This high unbinding free energy for sphingosine-1-phosphate underlines the observed specificity of the physiological effects of sphingosine-1-phosphate as it suggests that the spontaneous release of sphingosine-1-phosphate from apoM is unlikely.

12. results demonstrated that lower APOM levels in SLE patients and correlated with disease activity.

13. Sequenced the ApoM gene in recurrent venous thromboembolism (VTE) and identified six polymorphisms. ApoM rs805297 was significantly associated with higher risk of VTE recurrence in male but not in female patients.

14. Single nucleotide polymorphism in ApoM gene is associated with chronic obstructive pulmonary disease.

15. ApoM T-855C and T-778C polymorphisms were found to be associated with obesity by regulating HDL metabolism, and the T alleles of apoM T-778C were shown to be more strongly correlated.

16. liver mRNA levels of apoM and apoA1 decreased strongly upon sepsis induction.

17. 17beta-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-alpha-dependent pathway involving ER-alpha binding element in the promoter of the apoM gene.

18. A shift in ApoM/sphingosine 1-phosphate between HDL-particles in women with type 1 diabetes mellitus Is associated with impaired anti-inflammatory effects of the ApoM/S1P complex.

19. ApoM-bound sphingosine-1-phosphate regulates adhesion molecule abundance, leukocyte-endothelial adhesion, and endothelial barrier function via sphingosine-1-phosphate receptor1.

20. HDL-associated ApoM is anti-apoptotic by delivering sphingosine 1-phosphate to S1P1 and S1P3 receptors on vascular endothelium.

Mouse (Murine) Apolipoprotein M (APOM) interaction partners

1. this study shows that apolipoprotein M protects lipopolysaccharide-treated mice from death and organ injury

2. ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.

3. These results suggested that PPARgamma regulates the S1P levels by modulating apoM in a bell-shaped manner, with the greatest levels of apoM/S1P observed when PPARgamma was mildly expressed and that hepatic apoM/PPARgamma axis might maintain the homeostasis of S1P metabolism.

4. the data suggest that the phenotype of apoM-deficient mice is S1P dependent and reflects diminished S1P1 stimulation. The results reveal a link between the apoM/S1P axis and energy metabolism.

5. Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from high density lipoprotein-mediated cholesterol uptake in hepatocytes.

6. apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.

7. These S1P-induced enhancements in growth factors and chemotactic cytokines in retinal pigment epithelium cells were significantly inhibited by ApoM treatment. Additionally, in vivo experiments using a laser-induced choroidal neovascularization (CNV) murine model demonstrated that intravitreal ApoM injection significantly reduced the progression of CNV formation.

8. This study highlights the complexity of Apom/S1P in atherosclerosis and challenges the notion that the Apom/S1P complex is anti-atherogenic, at least in Apoe-deficient mice.

9. This suggests that the autophagy dysfunction caused by the deficiency of ApoM is an important factor in hepatic steatosis (triglyceride accumulation). ApoM plays a key role in normal autophagy activity in the liver and thereby further regulates the metabolism of liver lipids, particularly triglycerides.

10. HDL facilitates S1P efflux from erythrocytes by both apoM-dependent and apoM-independent mechanisms. Moreover, apoM facilitates tubular reabsorption of S1P from the urine, however, with no impact on S1P plasma concentrations.

11. The study suggests that vascular leakage of albumin-sized particles in ApoM deficiency is S1P- and S1P1-dependent and this dependency exacerbates the response to inflammatory stimuli.

12. apoM might facilitate the maintenance of CD4(+) T-lymphocytes or could modify the T-lymphocytes subgroups in murine spleen

13. Upon immune stimulation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier

14. LDL receptor and ApoE have roles in the clearance of ApoM-associated sphingosine 1-phosphate

15. ApoM augmented insulin secretion by maintaining the S1P concentration under both in vivo and in vitro conditions.

16. The present data indicate that the plasma apo-M levels modulate the ability of plasma to mobilize cellular cholesterol, whereas apo-M has no major effect on the excretion of cholesterol into feces.

17. ApoM can bind oxidized phospholipids, increasing the antioxidant effect of HDL.

18. Results show that apoM, by delivering S1P to the S1P(1) receptor on endothelial cells, is a vasculoprotective constituent of HDL.

19. After refolding from inclusion bodies, the crystal structure of apoM (reported here at 2.5 A resolution) displays a novel yet unprecedented seven-stranded beta-barrel structure.

20. apoM mainly associates with HDL in normal mice but also with the pathologically increased lipoprotein fraction in genetically modified mice; decreased apoM levels in apoA-I-deficient mice suggest a connection between apoM and apoA-I metabolism.