ArticleArteriosclerosis, thrombosis, and vascular biology2014
Ribosomal protein L13a deficiency in macrophages promotes atherosclerosis by limiting translation control-dependent retardation of inflammation.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Transient elevation in cellular glucose uptake exacerbates pressure overload-induced cardiac hypertrophy and dysfunction.Epigenetics · 2026Article
- Macrophage Differentiation Selectively Downregulates RPS15A While Preserving RPL13A and RPL17 Expression in THP-1-Derived Macrophages.Journal of cardiovascular development and disease · 2026Article
- Identification of biomarkers associated with mitochondria and macrophage polarization in acute myocardial infarction: a bioinformatics analysis and validation study.Journal of cardiothoracic surgery · 2026Article
- Article
- Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow.Journal of leukocyte biology · 2025Article
- Ribosomal proteins: the missing piece in the inflammation puzzle?Molecular and cellular biochemistry · 2025Review
- Toll-like receptor adaptor protein TIRAP has specialized roles in signaling, metabolic control and leukocyte migration upon wounding in zebrafish larvae.International journal of biological sciences · 2025Article
- The crosstalk between metabolism and translation.Cell metabolism · 2024Review
- High-throughput transcriptome profiling indicates ribosomal RNAs to be associated with resistance to immunotherapy in non-small cell lung cancer (NSCLC).Journal for immunotherapy of cancer · 2024Article
- Loss of function of ribosomal protein L13a blocks blastocyst formation and reveals a potential nuclear role in gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Ribosome biogenesis in disease: new players and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Re-Analysis of Single-Nucleus Transcriptomics Reveals Diverse Dorsal Root Ganglia Macrophage Responses Following Peripheral Nerve Injury.Biomedicines · 2022Article
- A Structurally Conserved RNA Element within SARS-CoV-2 ORF1a RNA and S mRNA Regulates Translation in Response to Viral S Protein-Induced Signaling in Human Lung Cells.Journal of virology · 2022Article
- Ribosomal Protein L13 Participates in Innate Immune Response Induced by Foot-and-Mouth Disease Virus.Frontiers in immunology · 2021Article
- BOP1 Knockdown Attenuates Neointimal Hyperplasia by Activating p53 and Inhibiting Nascent Protein Synthesis.Oxidative medicine and cellular longevity · 2021Article
- Shaping the Innate Immune Response Through Post-Transcriptional Regulation of Gene Expression Mediated by RNA-Binding Proteins.Frontiers in immunology · 2021Review
- Single cell transcriptomics of mouse kidney transplants reveals a myeloid cell pathway for transplant rejection.JCI insight · 2020Article
- High-fat diet-induced GAIT element-mediated translational silencing of mRNAs encoding inflammatory proteins in macrophage protects against atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mutually exclusive amino acid residues of L13a are responsible for its ribosomal incorporation and translational silencing leading to resolution of inflammation.RNA (New York, N.Y.) · 2019Article
- Activation of the unfolded protein response in high glucose treated endothelial cells is mediated by methylglyoxal.Scientific reports · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveUnresolved inflammatory response of macrophages plays a pivotal role in the pathogenesis of atherosclerosis. Previously we showed that ribosomal protein L13a-dependent translational silencing suppresses the synthesis of a cohort of inflammatory proteins in monocytes and macrophages. We also found that genetic abrogation of L13a expression in macrophages significantly compromised the resolution of inflammation in a mouse model of lipopolysaccharide-induced endotoxemia. However, its function in the pathogenesis of atherosclerosis is not known. Here, we examine whether L13a in macrophage has a protective role against high-fat diet-induced atherosclerosis. APPROACH AND
resultsWe bred the macrophage-specific L13a knockout mice L13a Flox(+/+) Cre(+/+) onto apolipoprotein E-deficient background and generated the experimental double knockout mice L13a Flox(+/+) Cre(+/+) apolipoprotein E deficient (apoE(-/-)). L13a Flox(+/+) Cre(-/-) mice on apolipoprotein E-deficient background were used as controls. Control and knockout mice were subjected to high-fat diet for 10 weeks. Evaluation of aortic sinus sections and entire aorta by en face showed significantly higher atherosclerosis in the knockout mice. Severity of atherosclerosis in knockout mice was accompanied by thinning of the smooth muscle cell layer in the media, larger macrophage area in the intimal plaque region and higher plasma levels of inflammatory cytokines. In addition, macrophages isolated from knockout mice had higher polyribosomal abundance of several target mRNAs, thus showing defect in translation control.
conclusionsOur data demonstrate that loss of L13a in macrophages increases susceptibility to atherosclerosis in apolipoprotein E-deficient mice, revealing an important role of L13a-dependent translational control as an endogenous protection mechanism against atherosclerosis.
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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.