ArticleThe Journal of biological chemistry2015
A solute carrier family 22 member 3 variant rs3088442 G→A associated with coronary heart disease inhibits lipopolysaccharide-induced inflammatory response.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
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- SLC22A3 deficiency leads to cognitive impairment through the cardio-neuroinflammatory axis mediated HA/H1R/NLRP3 pathway in heart failure mice.Redox biology · 2026Article
- Comprehensive Analysis of Bulk RNA-seq, Machine Learning, Mendelian Randomization, and Single-Cell Sequencing Unravels SLC22A3 as a Solute Carrier Superfamily-Associated Biomarker in Atherosclerosis.Journal of cardiovascular translational research · 2026Article
- Identification of Mitophagy-Related Genes and Analysis of Immune Infiltration in Atherosclerosis.Journal of inflammation research · 2025Article
- The epithelialProceedings of the National Academy of Sciences of the United States of America · 2024Article
- SLC38A2 promotes cell proliferation and invasion by promoting glutamine metabolism in adenomyosis.Experimental and therapeutic medicine · 2024Article
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- Chronic administration of glucocorticoid receptor ligands increases anxiety-like behavior and selectively increase serotonin transporters in the ventral hippocampus.Brain research · 2023Article
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- Oxygenized Low-Density Lipoprotein-Induced ASMC Dysregulation Depends on circ_0000345-Mediated Regulatory Mechanism.Journal of atherosclerosis and thrombosis · 2022Article
- High Throughput Screening of a Prescription Drug Library for Inhibitors of Organic Cation Transporter 3, OCT3.Pharmaceutical research · 2022Article
- Integrated Analysis of Gene Expression and Methylation Data to Identify Potential Biomarkers Related to Atherosclerosis Onset.Oxidative medicine and cellular longevity · 2022Article
- Association of Genetic Variants in miR-217 Gene with Risk of Coronary Artery Disease: A Case-Control Study.Pharmacogenomics and personalized medicine · 2021Article
- Genetic and Epigenetic Regulation of Organic Cation Transporters.Handbook of experimental pharmacology · 2021Review
- Organic Cation Transporters in Brain Catecholamine Homeostasis.Handbook of experimental pharmacology · 2021Review
- MiR-147: Functions and Implications in Inflammation and Diseases.MicroRNA (Shariqah, United Arab Emirates) · 2021Review
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- Effect ofFrontiers in cardiovascular medicine · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent genome-wide association studies have identified single-nucleotide polymorphism (SNPs) within the SLC22A3 (solute carrier family 22 member 3) gene associated with coronary heart disease (CHD) in the Caucasian population. We performed molecular analysis to investigate the potential role of SLC22A3 variants in CHD. Our study showed that the common polymorphism rs3088442 G→A, which is localized in the 3' UTR of the SLC22A3 gene, was associated with a decreased risk of CHD in the Chinese population by a case control study. In silico analysis indicated that G→A substitution of SNP rs3088442 created a putative binding site for miR-147 in the SLC22A3 mRNA. By overexpressing miR-147 or inhibiting endogenous miR-147, we demonstrated that SNP rs3088442 G→A recruited miR-147 to inhibit SLC22A3 expression. Moreover, SLC22A3 deficiency significantly decreased LPS-induced monocytic inflammatory response by interrupting NF-κB and MAPK signaling cascades in a histamine-dependent manner. Notably, the expression of SLC22A3(A) was also suppressed by LPS stimulus. Our findings might indicate a negative feedback mechanism against inflammatory response by which SLC22A3 polymorphisms decreased the risk of CHD.
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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 Socratic graph.