ArticleClinical and experimental immunology2015
Mechanism of glutamine inhibition of cytosolic phospholipase a2 (cPLA2 ): Evidence of physical interaction between glutamine-Induced mitogen-activated protein kinase phosphatase-1 and cPLA2.
Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Glutaminolysis is a Potential Therapeutic Target for Kidney Diseases.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Glutamine inhibits inflammation, oxidative stress, and apoptosis and ameliorates hyperoxic lung injury.Journal of physiology and biochemistry · 2023Article
- Glutamine deficiency shifts the asthmatic state toward neutrophilic airway inflammation.Allergy · 2022Article
- The effects of myelin on macrophage activation are phenotypic specific via cPLAScientific reports · 2021Article
- Lipid composition of the cancer cell membrane.Journal of bioenergetics and biomembranes · 2020Review
- Article
- Exogenous Glutamine in Respiratory Diseases: Myth or Reality?Nutrients · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-essential amino acid L-glutamine (Gln) possesses anti-inflammatory activity via deactivating cytosolic phospholipase A2 (cPLA2 ). We showed previously that Gln deactivated cPLA2 indirectly via dephosphorylating p38 mitogen-activated protein kinase (MAPK), the major kinase for cPLA2 phosphorylation, through inducing MAPK phosphatase-1 (MKP-1). In this study, we investigated the precise mechanism underlying Gln deactivation of cPLA2 . In lipopolysaccharide (LPS)-treated mice, Gln injection resulted in dephosphorylation of phosphorylated cPLA2 (p-cPLA2 ), which coincided with rapid Gln induction of MKP-1. MKP-1 small interfering RNA (siRNA) abrogated the ability of Gln to induce MKP-1 as well as the dephosphorylation of cPLA2 . Co-immunoprecipitation and in-situ proximity ligation assay revealed a physical interaction between MKP-1 and p-cPLA2 . In a murine model of allergic asthma, we also demonstrated the physical interaction between MKP-1 and p-cPLA2 . Furthermore, Gln suppressed various allergic asthma phenotypes, such as neutrophil and eosinophil recruitments into the airway, airway levels of T helper type 2 (Th2) cytokines [interleukin (IL)-4, IL-5 and IL-13], airway hyperresponsiveness, mucin production and metabolites (leukotriene B4 and platelet-activating factor) through inhibiting cPLA2 in a MKP-1-dependent manner. These data suggest that MKP-1 uses cPLA2 , in addition to p38, as a substrate, which further potentiates the anti-inflammatory action of Gln.
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Registered trials
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