ArticleJournal of molecular medicine (Berlin, Germany)2020
Autotaxin stimulates LPA2 receptor in macrophages and exacerbates dextran sulfate sodium-induced acute colitis.
Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Potential for anti‑angiogenic therapy targeting the receptor for advanced glycation end products/VEGF axis in ulcerative colitis (Review).Molecular medicine reports · 2026Review
- Autotaxin Induces S1P/S1PR1 Signaling to Affect Th17/Treg Cell Balance and Exacerbate Intestinal Inflammation in Colitis.International journal of molecular sciences · 2026Article
- YAP mediates HIV-related liver fibrosis.JHEP reports : innovation in hepatology · 2024Article
- Autotaxin inhibition attenuates the aortic valve calcification by suppressing inflammation-driven fibro-calcific remodeling of valvular interstitial cells.BMC medicine · 2024Article
- A dual role of lysophosphatidic acid type 2 receptor (LPAR2) in nonsteroidal anti-inflammatory drug-induced mouse enteropathy.Acta pharmacologica Sinica · 2024Article
- Tadalafil Enhances the Therapeutic Efficacy of Mesenchymal Stem Cells-Derived Exosomes in Pulmonary Hypertension by Upregulating miR-29a-3p.International journal of nanomedicine · 2024Article
- Emerging Roles of Lysophosphatidic Acid in Macrophages and Inflammatory Diseases.International journal of molecular sciences · 2023Review
- A type IV Autotaxin inhibitor ameliorates acute liver injury and nonalcoholic steatohepatitis.EMBO molecular medicine · 2022Article
- Fibrotic Response of Human Trabecular Meshwork Cells to Transforming Growth Factor-Beta 3 and Autotaxin in Aqueous Humor.Biomolecules · 2022Article
- Exploring the Molecular Mechanism of Tong Xie Yao Fang in Treating Ulcerative Colitis Using Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Tong Xie Yao Fang: A Classic Chinese Medicine Prescription with Potential for the Treatment of Ulcerative Colitis.Evidence-based complementary and alternative medicine : eCAM · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autotaxin (ATX) is a secreted enzyme that hydrolyzes lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA) and choline. ATX has been implicated in multiple chronic inflammatory diseases, but little is known about its role in the development of inflammatory bowel disease (IBD). Here, we investigated how ATX contributed to intestinal inflammation during colitis. We found that ATX expression levels were upregulated in the intestines of ulcerative colitis (UC) patients in acute state as well as in the intestines of dextran sulfate sodium (DSS)-induced colitis mice, which is likely due to increased infiltration of inflammatory cells including macrophages. Intriguingly, the inhibition of ATX activity led to reduced production of inflammatory cytokines, as well as attenuated colitis. These findings suggest that ATX may display strong pro-inflammatory properties. Supporting this, treatment with recombinant mouse ATX (rmATX) increased the production of inflammatory cytokines and enzymes in mouse macrophage cell line RAW264.7 and bone marrow-derived macrophages (BMDM), whereas silencing ATX by siRNA reduced LPS-stimulated production of pro-inflammatory factors. Notably, we found that the levels of LPA2 (an LPA receptor) were dramatically upregulated in rmATX-treated RAW264.7 cells and DSS-treated mice. Gene silencing of lpa2 in RAW264.7 cells by siRNA led to reduced production of inflammatory cytokines. Moreover, adenovirus-mediated delivery of lpa2 short hairpin RNA into DSS-treated mice ameliorated colitis. Collectively, our research suggests that ATX may exacerbate DSS-induced colitis by activating LPA2 receptor in macrophages and represent a promising target for the treatment of IBD. KEY MESSAGES: Increased ATX expression and secretion in colitic colons are likely due to increased infiltration of inflammatory cells including macrophages. Recombinant ATX promotes, but ATX silencing inhibits, the production of inflammatory cytokines in LPS-stimulated RAW264.7 cells and BMDM. •LPA2 mediates the pro-inflammatory effects of ATX on macrophages. Inhibition of ATX and downregulation of LPA2 ameliorate DSS-induced colitis.
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