ArticleExperimental and therapeutic medicine2023
LPS inhibits TRIM65 expression in macrophages and C57BL/6J mouse by activating the ERK1/2 signaling pathway.
Article in Experimental and therapeutic medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Potential Therapeutic Roles of Icariin in Inflammatory Diseases: From Molecular Mechanisms to Clinical Translation Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Tumor-derived HMGB2 induces M2-like macrophage polarization via TRIM65-mediated NLRP3 degradation to promote DLBCL progression.Journal for immunotherapy of cancer · 2026Article
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- Emerging Role of Calycosin in Inflammatory Diseases: Molecular Mechanisms and Potential Therapeutic Applications.Biomolecules · 2025Review
- Article
- Okra polysaccharide mitigates carrageenan-induced thrombosis in mice by regulating inflammation and oxidative stress.Frontiers in pharmacology · 2025Article
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Baicalin reduces sunitinib-induced cardiotoxicity in renal carcinoma PDX model by inhibiting myocardial injury, apoptosis and fibrosis.Frontiers in pharmacology · 2025Article
- The Role of Tripartite Motif Family Proteins in Chronic Liver Diseases: Molecular Mechanisms and Therapeutic Potential.Biomolecules · 2024Review
- E3 ligase TRIM65 alleviates intestinal ischemia/reperfusion injury through inhibition of TOX4-mediated apoptosis.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activated macrophages serve a key role in various inflammatory diseases, such as atherosclerosis and septic shock. Tripartite motif-containing protein 65 (TRIM65) has been previously reported to participate in tumor progression and lung inflammation. However, the molecular mechanisms that controls its expression under inflammatory conditions and its consequences in activated macrophages remain poorly understood. The present study first collected the tissues of C57BL/6J mice, smooth muscle cells, macrophages and endothelial cells to determine the expression and distribution of TRIM65 by reverse transcription-quantitative (RT-q) PCR and western blotting. Mouse and human macrophages were treated with LPS and C57BL/6J mice were intraperitoneally injected with LPS followed by isolation of spleen, lung, aorta and bone marrow. Following treatment, TRIM65 mRNA and protein level was examined by RT-qPCR and western blotting. The results showed that TRIM65 was highly expressed in organs of the immune system, such as the spleen, lymph node and thymus, but lowly expressed in heart, liver, brain and kidneys. TRIM65 was also highly expressed in macrophages and endothelial cells. TRIM65 mRNA and protein expression levels were found to be decreased in LPS-treated macrophages
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