ArticleThe Journal of biological chemistry2008
Prointerleukin-18 is activated by meprin beta in vitro and in vivo in intestinal inflammation.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 107 citations in OpenAlex.
- Meprin β is specifically inhibited by its cognate synthetic propeptide.Cellular and molecular life sciences : CMLS · 2026Article
- Meprin proteases in cutaneous homeostasis and psoriasis: pathophysiological mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- DNA remnants in red blood cells enable early detection of cancer.Cell research · 2025Article
- Meprin β regulates osteopontin-signaling in ischemia/reperfusion-induced kidney injury.BMC nephrology · 2025Article
- Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024Review
- Protein biomarkers in assessing kidney quality before transplantation‑current status and future perspectives (Review).International journal of molecular medicine · 2024Review
- Review
- ThePolymers · 2024Review
- Theranostic Fluorescent Probes.Chemical reviews · 2024Review
- Synthesis and structure-activity relationships of pyrazole-based inhibitors of meprin α and β.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- The trigger for pancreatic disease: NLRP3 inflammasome.Cell death discovery · 2023Review
- IL-18 in Autoinflammatory Diseases: Focus on Adult Onset Still Disease and Macrophages Activation Syndrome.International journal of molecular sciences · 2023Review
- A zebrafish HCT116 xenograft model to predict anandamide outcomes on colorectal cancer.Cell death & disease · 2022Article
- Helical ultrastructure of the metalloprotease meprin α in complex with a small molecule inhibitor.Nature communications · 2022Article
- Meprin β expression modulates the interleukin-6 mediated JAK2-STAT3 signaling pathway in ischemia/reperfusion-induced kidney injury.Physiological reports · 2022Article
- Heteroaromatic Inhibitors of the Astacin Proteinases Meprin α, Meprin β and Ovastacin Discovered by a Scaffold-Hopping Approach.ChemMedChem · 2021Article
- To be there when the picture is being painted.The Journal of biological chemistry · 2020Article
- Inhibiting the NLRP3 inflammasome with MCC950 ameliorates retinal neovascularization and leakage by reversing the IL-1β/IL-18 activation pattern in an oxygen-induced ischemic retinopathy mouse model.Cell death & disease · 2020Article
- NLRP3 Inflammasome-Mediated Inflammation in Acute Pancreatitis.International journal of molecular sciences · 2020Review
- Meprin-β activity modulates the β-catalytic subunit of protein kinase A in ischemia-reperfusion-induced acute kidney injury.American journal of physiology. Renal physiology · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin-18 (IL-18), a pro-inflammatory cytokine, is a key factor in inflammatory bowel disease (IBD). Caspase-1 activates this cytokine, but other proteases are likely involved in maturation. Because meprin metalloproteinases have been implicated in IBD, the interaction of these proteases with proIL-18 was studied. The results demonstrate that the meprin beta subunit of meprins A and B cleaves proIL-18 into a smaller 17-kDa product. The cleavage is at the Asn51-Asp52 bond, a site C-terminal to caspase-1 cleavage. The cleavage occurred in vitro with a Km of 1.3 microm and in Madin-Darby canine kidney cells transfected with meprin beta when proIL-18 was added to the culture medium. The product of meprin B cleavage of proIL-18 activated NF-kappaB in EL-4 cells, indicating that it was biologically active. To determine the physiological significance of the interactions of meprins with proIL-18, an experimental model of IBD was produced by administering dextran sulfate sodium (DSS) to wild-type and meprin beta knock-out (betaKO) mice, and the serum levels of active IL-18 were determined. DSS-treated meprin betaKO mice had lower levels of the active cytokine in the serum compared with wild-type mice. Furthermore, in meprin alphaKO mice, which express meprin beta but not alpha, active IL-18 was elevated in the serum of DSS-treated mice compared with wild-type mice, indicating that the meprin isoforms have opposing effects on the IL-18 levels in vivo. This study identifies proIL-18 as a biologically important substrate for meprin beta and implicates meprins in the modulation of inflammation.
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