Interactions between lysophosphatidylinositol receptor GPR55 and sphingosine-1-phosphate receptor S1P5 in live cells

Hong, Hahoon; Yoon, Byoung-Su; Ghil, Sungho

doi:10.1016/j.bbrc.2021.07.032

Cited by 6 publications

(5 citation statements)

References 34 publications

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“…We suggest, based on the reported functional role of LPI 20:4 in immune response and cancer progression [92], that the reason cells that circulate in the plasma of DLBCL (tumour + TME cells) produce more LPI 20:4 is to sustain cancer cell growth and evade the host immune response. A recent research established a link between activated S1P receptor and LPI receptor GPR55, which interacted strongly and specifically, both being erroneously expressed in many cancer types [93]. Hence, the augmented plasma levels of both S1P and LPI 20:4 in DLBCL detected in our study (Table 3) point towards a concerted modulation of the GPR55 by S1P and LPI.…”

Section: Discussionsupporting

confidence: 58%

Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

Masnikosa,

Pirić,

Post

et al. 2023

Cancers

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Lipidome dysregulation is a hallmark of cancer and inflammation. The global plasma lipidome and sub-lipidome of inflammatory pathways have not been reported in diffuse large B-cell lymphoma (DLBCL). In a pilot study of plasma lipid variation in female DLBCL patients and BMI-matched disease-free controls, we performed targeted lipidomics using LC-MRM to quantify lipid mediators of inflammation and immunity, and those known or hypothesised to be involved in cancer progression: sphingolipids, resolvin D1, arachidonic acid (AA)-derived oxylipins, such as hydroxyeicosatetraenoic acids (HETEs) and dihydroxyeicosatrienoic acids, along with their membrane structural precursors. We report on the role of the eicosanoids in the separation of DLBCL from controls, along with lysophosphatidylinositol LPI 20:4, implying notable changes in lipid metabolic and/or signalling pathways, particularly pertaining to AA lipoxygenase pathway and glycerophospholipid remodelling in the cell membrane. We suggest here the set of S1P, SM 36:1, SM 34:1 and PI 34:1 as DLBCL lipid signatures which could serve as a basis for the prospective validation in larger DLBCL cohorts. Additionally, untargeted lipidomics indicates a substantial change in the overall lipid metabolism in DLBCL. The plasma lipid profiling of DLBCL patients helps to better understand the specific lipid dysregulations and pathways in this cancer.

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Section: Discussionsupporting

confidence: 58%

Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

Masnikosa,

Pirić,

Post

et al. 2023

Cancers

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“…The data suggest that, besides the actions of GPR55 and CB2 receptors alone, the formation of GPR55-CB2 dimers could participate in the expression of cytokine genes triggered by LPI. GPR55 receptor interaction with distinct GPCRs, such as the S1PR [ 43 ] and the lysophosphatidic acid (LPA) 2 receptor [ 44 ], has been demonstrated in some cell preparations. Specifically, GPR55 dimer formation with cannabinoid receptors has been previously observed in neutrophils, transfected HEK293 cells, and cancer cells [ 18 , 45 , 46 ].…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidylinositol Promotes Chemotaxis and Cytokine Synthesis in Mast Cells with Differential Participation of GPR55 and CB2 Receptors

Martínez-Aguilar

Ibarra-Sánchez

Guerrero-Morán

et al. 2023

IJMS

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Mast cells (MCs) are the main participants in the control of immune reactions associated with inflammation, allergies, defense against pathogens, and tumor growth. Bioactive lipids are lipophilic compounds able to modulate MC activation. Here, we explored some of the effects of the bioactive lipid lysophosphatidylinositol (LPI) on MCs. Utilizing murine bone marrow-derived mast cells (BMMCs), we found that LPI did not cause degranulation, but slightly increased FcεRI-dependent β-hexosaminidase release. However, LPI induced strong chemotaxis together with changes in LIM kinase (LIMK) and cofilin phosphorylation. LPI also promoted modifications to actin cytoskeleton dynamics that were detected by an increase in cell size and interruptions in the continuity of the cortical actin ring. The chemotaxis and cortical actin ring changes were dependent on GPR55 receptor activation, since the specific agonist O1602 mimicked the effects of LPI and the selective antagonist ML193 prevented them. The LPI and O1602-dependent stimulation of BMMC also led to VEGF, TNF, IL-1α, and IL-1β mRNA accumulation, but, in contrast with chemotaxis-related processes, the effects on cytokine transcription were dependent on GPR55 and cannabinoid (CB) 2 receptors, since they were sensitive to ML193 and to the specific CB2 receptor antagonist AM630. Remarkably, GPR55-dependent BMMC chemotaxis was observed towards conditioned media from distinct mouse and human cancer cells. Our data suggest that LPI induces the chemotaxis of MCs and leads to cytokine production in MC in vitro with the differential participation of GPR55 and CB2 receptors. These effects could play a significant role in the recruitment of MCs to tumors and the production of MC-derived pro-angiogenic factors in the tumor microenvironment.

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“…Indeed, similar disparities between changes in mRNA abundance and protein content have been already reported [ 56 ], also within the ECS, by others [ 57 ] and by us [ 58 , 59 ]. Interestingly, an interaction between GPR55 and S1P5 receptor has already been demonstrated in a colon cancer cell line [ 60 ]. In particular, S1P5 strongly and specifically interacts with GPR55, and the activation of each receptor led to increased cell proliferation, ERK phosphorylation and cancer-associated gene expression.…”

Section: Discussionmentioning

confidence: 99%

“…In particular, S1P5 strongly and specifically interacts with GPR55, and the activation of each receptor led to increased cell proliferation, ERK phosphorylation and cancer-associated gene expression. Conversely, co-activation of both receptors inhibited the above mentioned events, supporting the occurrence of a functional crosstalk [ 60 ]. In the herein-investigated model of murine myoblasts, S1P significantly rearranges cell sensitivity to eCBs without changing their endogenous content, suggesting a potential impact on the signal transduction driven by these lipid mediators.…”

Section: Discussionmentioning

confidence: 99%

The TRPV1 Receptor Is Up-Regulated by Sphingosine 1-Phosphate and Is Implicated in the Anandamide-Dependent Regulation of Mitochondrial Activity in C2C12 Myoblasts

Standoli

Pecchioli

Tortolani

et al. 2022

IJMS

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The sphingosine 1-phosphate (S1P) and endocannabinoid (ECS) systems comprehend bioactive lipids widely involved in the regulation of similar biological processes. Interactions between S1P and ECS have not been so far investigated in skeletal muscle, where both systems are active. Here, we used murine C2C12 myoblasts to investigate the effects of S1P on ECS elements by qRT-PCR, Western blotting and UHPLC-MS. In addition, the modulation of the mitochondrial membrane potential (ΔΨm), by JC-1 and Mitotracker Red CMX-Ros fluorescent dyes, as well as levels of protein controlling mitochondrial function, along with the oxygen consumption were assessed, by Western blotting and respirometry, respectively, after cell treatment with methanandamide (mAEA) and in the presence of S1P or antagonists to endocannabinoid-binding receptors. S1P induced a significant increase in TRPV1 expression both at mRNA and protein level, while it reduced the protein content of CB2. A dose-dependent effect of mAEA on ΔΨm, mediated by TRPV1, was evidenced; in particular, low doses were responsible for increased ΔΨm, whereas a high dose negatively modulated ΔΨm and cell survival. Moreover, mAEA-induced hyperpolarization was counteracted by S1P. These findings open new dimension to S1P and endocannabinoids cross-talk in skeletal muscle, identifying TRPV1 as a pivotal target.

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Interactions between lysophosphatidylinositol receptor GPR55 and sphingosine-1-phosphate receptor S1P5 in live cells

Cited by 6 publications

References 34 publications

Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

Lysophosphatidylinositol Promotes Chemotaxis and Cytokine Synthesis in Mast Cells with Differential Participation of GPR55 and CB2 Receptors

The TRPV1 Receptor Is Up-Regulated by Sphingosine 1-Phosphate and Is Implicated in the Anandamide-Dependent Regulation of Mitochondrial Activity in C2C12 Myoblasts

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