ArticleDNA and cell biology2015
ApoM Suppresses TNF-α-Induced Expression of ICAM-1 and VCAM-1 Through Inhibiting the Activity of NF-κB.
Article in DNA and cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- The Inflammatory Potential of Dietary Manganese in a Cohort of Elderly Men.Biological trace element research · 2018Trial
- Molecular characteristics of apolipoprotein M and its biological functions in kidney diseases.Molecular and cellular biochemistry · 2026Review
- NF-κB/ICAM-1 signaling regulates vascular dysfunction in depressive hypertension rats.Scientific reports · 2025Article
- Article
- Plasma apolipoprotein M predicts overall survival in metastatic breast cancer patients.Breast cancer research and treatment · 2023Article
- DNA-dependent protein kinase catalytic subunit binds to the transactivation domain 1 of NF-κB p65.Biochemistry and biophysics reports · 2023Article
- Evaluation of the anti-gout effect ofMedicine and pharmacy reports · 2021Article
- Increased expression levels of inflammatory cytokines and adhesion molecules in lipopolysaccharide‑induced acute inflammatory apoM‑/‑ mice.Molecular medicine reports · 2020Article
- Niaspan inhibits diabetic retinopathy‑induced vascular inflammation by downregulating the tumor necrosis factor‑α pathway.Molecular medicine reports · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the anti-inflammatory effect of apolipoprotein M (apoM) on regulation of tumor necrosis factor-α (TNF-α)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and further investigate the molecular mechanism of apoM in this process. We found that TNF-α could decrease expression of apoM and inhibitor of NF-κB-α (IκBα) in HepG2 cells. Overexpression of apoM caused a significant decrease of ICAM-1 and VCAM-1 expression, while it caused a significant increase of IκBα expression in HepG2 cells. Furthermore, the treatment with TNF-α could increase ICAM-1 and VCAM-1 expression, decrease IκBα protein expression, and increase nuclear factor-κB (NF-κB) activity, and these effects were markedly enhanced by small interfering RNA (siRNA)-mediated silencing of apoM in HepG2 cells. Our findings demonstrated that apoM suppressed TNF-α-induced expression of ICAM-1 and VCAM-1 through inhibiting the activity of NF-κB.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.