ArticleBMC cardiovascular disorders2019
Apolipoprotein M and sphingosine-1-phosphate complex alleviates TNF-α-induced endothelial cell injury and inflammation through PI3K/AKT signaling pathway.
Article in BMC cardiovascular disorders, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- Tetrahydrocurcumin for Major Depressive Disorder with Therapeutic Potential and Mechanistic Insights from Clinical and Preclinical Studies.Molecular neurobiology · 2025Trial
- Physcion-8-O-β-D-monoglucoside protects hepatocytes from TNF-α-mediated apoptosis by suppressing the PI3K/AKT/NF-κB signaling pathway.Scientific reports · 2026Article
- Targeting pyroptosis in atherosclerosis: emerging pharmacologic strategies and natural compound-based therapeutics-a narrative review.International journal of clinical pharmacy · 2026Review
- RETRACTION: Hydroxysafflor Yellow A Inhibits TNF-Evidence-based complementary and alternative medicine : eCAM · 2026Article
- Inventive HDL Mimicking Nanoparticles: A Promising Frontier in Cardiovascular Disease Management.Cardiovascular toxicology · 2025Review
- ApoM maintains cellular homeostasis between mitophagy and apoptosis by affecting the stability of Nnt mRNA through the Zic3-ApoM-Elavl2-Nnt axis during neural tube closure.Cell death & disease · 2025Article
- FSH Is Responsible for Androgen Deprivation Therapy-Associated Atherosclerosis in Mice by Exaggerating Endothelial Inflammation and Monocyte Adhesion.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- The role of sphingosine-1-phosphate in autophagy and related disorders.Cell death discovery · 2023Review
- Hydrogen sulfide ameliorates abdominal aorta coarctation-induced myocardial fibrosis by inhibiting pyroptosis through regulating eukaryotic translation initiation factor 2α phosphorylation and activating PI3K/AKT1 pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- HDL Function and Atherosclerosis: Reactive Dicarbonyls as Promising Targets of Therapy.Circulation research · 2023Review
- Dietary Evodiamine Inhibits Atherosclerosis-Associated Changes in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2023Article
- Lipocalin family proteins and their diverse roles in cardiovascular disease.Pharmacology & therapeutics · 2023Review
- Knockdown of the long non‑coding RNA MALAT1 ameliorates TNF‑α‑mediated endothelial cell pyroptosis via the miR‑30c‑5p/Cx43 axis.Molecular medicine reports · 2023Article
- Pyroptosis-triggered pathogenesis: New insights on antiphospholipid syndrome.Frontiers in immunology · 2023Review
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
- The role of sphingosine-1-phosphate in the development and progression of Parkinson's disease.Frontiers in cellular neuroscience · 2023Review
- Sphingolipids in mitochondria-from function to disease.Frontiers in cell and developmental biology · 2023Review
- Interactions between PCSK9 and NLRP3 inflammasome signaling in atherosclerosis.Frontiers in immunology · 2023Review
- The emerging role of pyroptosis-related inflammasome pathway in atherosclerosis.Molecular medicine (Cambridge, Mass.) · 2022Review
- Effects of sphingolipid metabolism disorders on endothelial cells.Lipids in health and disease · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn spite of the important role of Apolipoprotein-M (ApoM) and Sphingosine-1-Phosphate (S1P) played in atherosclerosis (AS), there was few related research reporting ApoM and S1P complex (ApoM-S1P) on biological activities of human umbilical vein endothelial cells (HUVECs). In this study, we explored the effect and mechanism of ApoM-S1P on TNF-α-induced inflammation in HUVECs.
methodsTNF-α was utilized to induce HUVEC injury and inflammation. After HUVECs were treated with antagonists of ApoM, S1P, ApoM + S1P, and ApoM + S1P + S1PR, calcein-acetoxymethyl ester was employed for the assessment of the adhesion of HUVECs to THP-1, immunofluorescence for the observation of caspase-1expression in HUVECs, reactive oxygen species (ROS) kit for the detection of ROS level in HUVECs. The impact of TNF-α, ApoM, S1P and S1PR antagonists on inflammatory response, pyroptosis and adhesion of THP-1 monocytes to HUVECs were determined by detecting expressions of pyroptosis related proteins (IL-1β, IL-18, ASC, NLRP3 and caspase-1), inflammatory cytokines (IL-6 and IL-10), adhesion molecules (E-selectin, ICAM-1, and VCAM-1) and p-PI3K/p-AKT by qRT-PCR and Western blot, as well as by ELISA.
resultsTNF-α could increase adhesion of THP-1 monocytes to HUVECs and induce inflammatory response and pyroptosis in HUVECs, indicated by up-regulated expressions of E-selectin, ICAM-1, VCAM-1, IL-1β, IL-18, caspase-1, ASC, NLRP3, and IL-6, and down-regulated expression of IL-10. Co-treatment of ApoM-S1P on TNF-α treated HUVECs could protect HUVECs from injury and inflammation, evidenced by the attenuation of expressions of pyroptosis related proteins, inflammatory cytokines, and adhesion molecules, as well as the augment of PI3K and AKT phosphorylation. JTE-013, an antagonist of S1PR2, could reverse the amelioration of ApoM-S1P on pyroptosis and inflammation of HUVECs, indicating that ApoM-S1P could bind to S1PR2 to protect HUVECs from injury and inflammation through activating PI3K/AKT pathway.
conclusionApoM-S1P could attenuate TNF-α induced injury and inflammatory response in HUVECs by binding to S1PR2 to activate PI3K/AKT pathway.
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