Lysophosphatidylglucoside/GPR55 signaling promotes foam cell formation in human M2c macrophages.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
06 08 2023
Historique:
received: 26 04 2023
accepted: 01 08 2023
medline: 8 8 2023
pubmed: 7 8 2023
entrez: 6 8 2023
Statut: epublish

Résumé

Atherosclerosis is a major cause of cerebral and cardiovascular diseases. Intravascular plaques, a well-known pathological finding of atherosclerosis, have a necrotic core composed of macrophages and dead cells. Intraplaque macrophages, which are classified into various subtypes, play key roles in maintenance of normal cellular microenvironment. Excessive uptake of oxidized low-density lipoprotein causes conversion of macrophages to foam cells, and consequent progression/exacerbation of atherosclerosis. G-protein-coupled receptor 55 (GPR55) signaling has been reported to associate with atherosclerosis progression. We demonstrated recently that lysophosphatidylglucoside (lysoPtdGlc) is a specific ligand of GPR55, although in general physiological ligands of GPR55 are poorly understood. Phosphatidylglucoside is expressed on human monocytes and can be converted to lysoPtdGlc. In the present study, we examined possible involvement of lysoPtdGlc/GPR55 signaling in foam cell formation. In monocyte-derived M2c macrophages, lysoPtdGlc/GPR55 signaling inhibited translocation of ATP binding cassette subfamily A member 1 to plasma membrane, and cholesterol efflux. Such inhibitory effect was reversed by GPR55 antagonist ML193. LysoPtdGlc/GPR55 signaling in M2c macrophages was involved in excessive lipid accumulation, thereby promoting foam cell formation. Our findings suggest that lysoPtdGlc/GPR55 signaling is a potential therapeutic target for inhibition of atherosclerosis progression.

Identifiants

pubmed: 37544935
doi: 10.1038/s41598-023-39904-x
pii: 10.1038/s41598-023-39904-x
pmc: PMC10404585
doi:

Substances chimiques

Cholesterol 97C5T2UQ7J
Lipoproteins, LDL 0
ATP Binding Cassette Transporter 1 0
GPR55 protein, human 0
Receptors, Cannabinoid 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

12740

Informations de copyright

© 2023. Springer Nature Limited.

Références

Spitz, C. et al. Regulatory T cells in atherosclerosis: Critical immune regulatory function and therapeutic potential. Cell. Mol. Life Sci. 73, 901–922. https://doi.org/10.1007/s00018-015-2080-2 (2015).
doi: 10.1007/s00018-015-2080-2 pubmed: 26518635
Kiss, M. G. & Binder, C. J. The multifaceted impact of complement on atherosclerosis. Atherosclerosis 351, 29–40. https://doi.org/10.1016/j.atherosclerosis.2022.03.014 (2022).
doi: 10.1016/j.atherosclerosis.2022.03.014 pubmed: 35365353
Yokoi, H., Oda, E., Kaneko, K. & Matsubayashi, K. Duration and clinical outcome of dual antiplatelet therapy after percutaneous coronary intervention: A retrospective cohort study using a medical information database from Japanese hospitals. Cardiovasc Interv Ther 37, 465–474. https://doi.org/10.1007/s12928-021-00833-z (2022).
doi: 10.1007/s12928-021-00833-z pubmed: 35141843 pmcid: 9197891
Frostegard, J. Immunity, atherosclerosis and cardiovascular disease. BMC Med. 11, 117. https://doi.org/10.1186/1741-7015-11-117 (2013).
doi: 10.1186/1741-7015-11-117 pubmed: 23635324 pmcid: 3658954
Tabas, I. & Bornfeldt, K. E. Macrophage phenotype and function in different stages of atherosclerosis. Circ. Res. 118, 653–667. https://doi.org/10.1161/CIRCRESAHA.115.306256 (2016).
doi: 10.1161/CIRCRESAHA.115.306256 pubmed: 26892964 pmcid: 4762068
Xu, H., Jiang, J., Chen, W., Li, W. & Chen, Z. Vascular macrophages in atherosclerosis. J. Immunol. Res. 2019, 4354786. https://doi.org/10.1155/2019/4354786 (2019).
doi: 10.1155/2019/4354786 pubmed: 31886303 pmcid: 6914912
Mushenkova, N. V. et al. Functional phenotypes of intraplaque macrophages and their distinct roles in atherosclerosis development and atheroinflammation. Biomedicines https://doi.org/10.3390/biomedicines10020452 (2022).
doi: 10.3390/biomedicines10020452 pubmed: 35203661 pmcid: 8962399
Moore, K. J., Sheedy, F. J. & Fisher, E. A. Macrophages in atherosclerosis: A dynamic balance. Nat. Rev. Immunol. 13, 709–721. https://doi.org/10.1038/nri3520 (2013).
doi: 10.1038/nri3520 pubmed: 23995626 pmcid: 4357520
Willemsen, L. & de Winther, M. P. Macrophage subsets in atherosclerosis as defined by single-cell technologies. J. Pathol. 250, 705–714. https://doi.org/10.1002/path.5392 (2020).
doi: 10.1002/path.5392 pubmed: 32003464 pmcid: 7217201
Zizzo, G. & Cohen, P. L. IL-17 stimulates differentiation of human anti-inflammatory macrophages and phagocytosis of apoptotic neutrophils in response to IL-10 and glucocorticoids. J. Immunol. 190, 5237–5246. https://doi.org/10.4049/jimmunol.1203017 (2013).
doi: 10.4049/jimmunol.1203017 pubmed: 23596310
Calvillo-Robledo, A., Cervantes-Villagrana, R. D., Morales, P. & Marichal-Cancino, B. A. The oncogenic lysophosphatidylinositol (LPI)/GPR55 signaling. Life Sci. 301, 120596. https://doi.org/10.1016/j.lfs.2022.120596 (2022).
doi: 10.1016/j.lfs.2022.120596 pubmed: 35500681
Stančić, A. et al. The GPR55 antagonist CID16020046 protects against intestinal inflammation. Neurogastroenterol. Motil. 27, 1432–1445. https://doi.org/10.1111/nmo.12639 (2015).
doi: 10.1111/nmo.12639 pubmed: 26227635 pmcid: 4587547
Lanuti, M., Talamonti, E., Maccarrone, M. & Chiurchiu, V. Activation of GPR55 receptors exacerbates oxLDL-induced lipid accumulation and inflammatory responses, while reducing cholesterol efflux from human macrophages. PLoS ONE 10, e0126839. https://doi.org/10.1371/journal.pone.0126839 (2015).
doi: 10.1371/journal.pone.0126839 pubmed: 25970609 pmcid: 4430319
Lee, S. J. & Im, D. S. GPR55 antagonist CID16020046 protects against atherosclerosis development in mice by inhibiting monocyte adhesion and Mac-1 expression. Int. J. Mol. Sci. https://doi.org/10.3390/ijms222313084 (2021).
doi: 10.3390/ijms222313084 pubmed: 35008852 pmcid: 8745242
Kawano-Yamamoto, C. et al. Establishment and characterization of a new erythroblastic leukemia cell line, EEB: Phosphatidylglucoside-mediated erythroid differentiation and apoptosis. Leuk. Res. 30, 829–839. https://doi.org/10.1016/j.leukres.2005.10.021 (2006).
doi: 10.1016/j.leukres.2005.10.021 pubmed: 16332389
Oka, S. et al. Preferential expression of phosphatidylglucoside along neutrophil differentiation pathway. Leuk Lymphoma 50, 1190–1197. https://doi.org/10.1080/10428190902934928 (2009).
doi: 10.1080/10428190902934928 pubmed: 19557640
Kina, K. et al. The novel neutrophil differentiation marker phosphatidylglucoside mediates neutrophil apoptosis. J. Immunol. 186, 5323–5332. https://doi.org/10.4049/jimmunol.1002100 (2011).
doi: 10.4049/jimmunol.1002100 pubmed: 21451106
Nagatsuka, Y. et al. Carbohydrate-dependent signaling from the phosphatidylglucoside-based microdomain induces granulocytic differentiation of HL60 cells. Proc. Natl. Acad. Sci. U.S.A. 100, 7454–7459. https://doi.org/10.1073/pnas.1232503100 (2003).
doi: 10.1073/pnas.1232503100 pubmed: 12802014 pmcid: 164607
Li, X. et al. Lysophosphatidylglucoside is a GPR55 -mediated chemotactic molecule for human monocytes and macrophages. Biochem. Biophys. Res. Commun. 569, 86–92. https://doi.org/10.1016/j.bbrc.2021.06.090 (2021).
doi: 10.1016/j.bbrc.2021.06.090 pubmed: 34237432
Guy, A. T. et al. NEURONAL DEVELOPMENT. Glycerophospholipid regulation of modality-specific sensory axon guidance in the spinal cord. Science 349, 974–977. https://doi.org/10.1126/science.aab3516 (2015).
doi: 10.1126/science.aab3516 pubmed: 26315437
Hung, H. H. et al. Selective involvement of UGGT variant: UGGT2 in protecting mouse embryonic fibroblasts from saturated lipid-induced ER stress. Proc. Natl. Acad. Sci. U.S.A. 119, e2214957119. https://doi.org/10.1073/pnas.2214957119 (2022).
doi: 10.1073/pnas.2214957119 pubmed: 36508673 pmcid: 9907099
Ishiyama, J., Taguchi, R., Yamamoto, A. & Murakami, K. Palmitic acid enhances lectin-like oxidized LDL receptor (LOX-1) expression and promotes uptake of oxidized LDL in macrophage cells. Atherosclerosis 209, 118–124. https://doi.org/10.1016/j.atherosclerosis.2009.09.004 (2010).
doi: 10.1016/j.atherosclerosis.2009.09.004 pubmed: 19782984
Chistiakov, D. A., Bobryshev, Y. V. & Orekhov, A. N. Macrophage-mediated cholesterol handling in atherosclerosis. J. Cell Mol. Med. 20, 17–28. https://doi.org/10.1111/jcmm.12689 (2016).
doi: 10.1111/jcmm.12689 pubmed: 26493158
Oh, J. et al. Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation. J. Biol. Chem. 287, 11629–11641. https://doi.org/10.1074/jbc.M111.338673 (2012).
doi: 10.1074/jbc.M111.338673 pubmed: 22356914 pmcid: 3320912
Yu, X. H., Fu, Y. C., Zhang, D. W., Yin, K. & Tang, C. K. Foam cells in atherosclerosis. Clin. Chim. Acta 424, 245–252. https://doi.org/10.1016/j.cca.2013.06.006 (2013).
doi: 10.1016/j.cca.2013.06.006 pubmed: 23782937
Ghosh, S. Macrophage cholesterol homeostasis and metabolic diseases: Critical role of cholesteryl ester mobilization. Expert Rev. Cardiovasc. Ther. 9, 329–340. https://doi.org/10.1586/erc.11.16 (2011).
doi: 10.1586/erc.11.16 pubmed: 21438812 pmcid: 3098044
Calkin, A. C. & Tontonoz, P. Liver x receptor signaling pathways and atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 30, 1513–1518. https://doi.org/10.1161/ATVBAHA.109.191197 (2010).
doi: 10.1161/ATVBAHA.109.191197 pubmed: 20631351
Spann, N. J. et al. Regulated accumulation of desmosterol integrates macrophage lipid metabolism and inflammatory responses. Cell 151, 138–152. https://doi.org/10.1016/j.cell.2012.06.054 (2012).
doi: 10.1016/j.cell.2012.06.054 pubmed: 23021221 pmcid: 3464914
Remmerie, A. & Scott, C. L. Macrophages and lipid metabolism. Cell. Immunol. 330, 27–42. https://doi.org/10.1016/j.cellimm.2018.01.020 (2018).
doi: 10.1016/j.cellimm.2018.01.020 pubmed: 29429624 pmcid: 6108423
Schrijvers, D. M., De Meyer, G. R. Y., Kockx, M. M., Herman, A. G. & Martinet, W. Phagocytosis of apoptotic cells by macrophages is impaired in atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 25, 1256–1261. https://doi.org/10.1161/01.ATV.0000166517.18801.a7 (2005).
doi: 10.1161/01.ATV.0000166517.18801.a7 pubmed: 15831805
Jinnouchi, H. et al. Diversity of macrophage phenotypes and responses in atherosclerosis. Cell Mol. Life Sci. 77, 1919–1932. https://doi.org/10.1007/s00018-019-03371-3 (2020).
doi: 10.1007/s00018-019-03371-3 pubmed: 31720740
Kitamura, Y. et al. Immunohistochemical distribution of phosphatidylglucoside using anti-phosphatidylglucoside monoclonal antibody (DIM21). Biochem. Biophys. Res. Commun. 362, 252–255. https://doi.org/10.1016/j.bbrc.2007.07.065 (2007).
doi: 10.1016/j.bbrc.2007.07.065 pubmed: 17707337
Baidzajevas, K. et al. Macrophage polarisation associated with atherosclerosis differentially affects their capacity to handle lipids. Atherosclerosis 305, 10–18. https://doi.org/10.1016/j.atherosclerosis.2020.05.003 (2020).
doi: 10.1016/j.atherosclerosis.2020.05.003 pubmed: 32592946
Guerrini, V. & Gennaro, M. L. Foam cells: One size doesn’t fit all. Trends Immunol. 40, 1163–1179. https://doi.org/10.1016/j.it.2019.10.002 (2019).
doi: 10.1016/j.it.2019.10.002 pubmed: 31732284 pmcid: 6925453
Matsuo, M. ABCA1 and ABCG1 as potential therapeutic targets for the prevention of atherosclerosis. J. Pharmacol. Sci. 148, 197–203. https://doi.org/10.1016/j.jphs.2021.11.005 (2022).
doi: 10.1016/j.jphs.2021.11.005 pubmed: 35063134
Dubland, J. A. & Francis, G. A. Lysosomal acid lipase: At the crossroads of normal and atherogenic cholesterol metabolism. Front. Cell Dev. Biol. 3, 3. https://doi.org/10.3389/fcell.2015.00003 (2015).
doi: 10.3389/fcell.2015.00003 pubmed: 25699256 pmcid: 4313778
Singaraja, R. R. et al. Palmitoylation of ATP-binding cassette transporter A1 is essential for its trafficking and function. Circ. Res. 105, 138–147. https://doi.org/10.1161/CIRCRESAHA.108.193011 (2009).
doi: 10.1161/CIRCRESAHA.108.193011 pubmed: 19556522
Fitzgerald, M. L. et al. ATP-binding cassette transporter A1 contains an NH
doi: 10.1074/jbc.m100474200 pubmed: 11328826
Neufeld, E. B. et al. Cellular localization and trafficking of the human ABCA1 transporter. J. Biol. Chem. 276, 27584–27590. https://doi.org/10.1074/jbc.M103264200 (2001).
doi: 10.1074/jbc.M103264200 pubmed: 11349133
Quazi, F. & Molday, R. S. Differential phospholipid substrates and directional transport by ATP-binding cassette proteins ABCA1, ABCA7, and ABCA4 and disease-causing mutants. J. Biol. Chem. 288, 34414–34426. https://doi.org/10.1074/jbc.M113.508812 (2013).
doi: 10.1074/jbc.M113.508812 pubmed: 24097981 pmcid: 3843056
Kasza, I. et al. Model system for the analysis of cell surface expression of human ABCA1. BMC Cell Biol. 10, 93. https://doi.org/10.1186/1471-2121-10-93 (2009).
doi: 10.1186/1471-2121-10-93 pubmed: 20025763 pmcid: 2804593
Haidar, B., Denis, M., Krimbou, L., Marcil, M. & Genest, J. Jr. cAMP induces ABCA1 phosphorylation activity and promotes cholesterol efflux from fibroblasts. J. Lipid Res. 43, 2087–2094. https://doi.org/10.1194/jlr.m200235-jlr200 (2002).
doi: 10.1194/jlr.m200235-jlr200 pubmed: 12454270
Kavurma, M. M., Bhindi, R., Lowe, H. C., Chesterman, C. & Khachigian, L. M. Vessel wall apoptosis and atherosclerotic plaque instability. J. Thromb. Haemost. 3, 465–472. https://doi.org/10.1111/j.1538-7836.2005.01120.x (2005).
doi: 10.1111/j.1538-7836.2005.01120.x pubmed: 15748235
Kong, P. et al. Inflammation and atherosclerosis: Signaling pathways and therapeutic intervention. Signal Transduct. Target Ther. 7, 131. https://doi.org/10.1038/s41392-022-00955-7 (2022).
doi: 10.1038/s41392-022-00955-7 pubmed: 35459215 pmcid: 9033871
Wang, Y., Pan, W., Wang, Y. & Yin, Y. The GPR55 antagonist CID16020046 protects against ox-LDL-induced inflammation in human aortic endothelial cells (HAECs). Arch. Biochem. Biophys. 681, 108254. https://doi.org/10.1016/j.abb.2020.108254 (2020).
doi: 10.1016/j.abb.2020.108254 pubmed: 31904362
Rinne, P. et al. Palmitoylethanolamide promotes a proresolving macrophage phenotype and attenuates atherosclerotic plaque formation. Arterioscler. Thromb. Vasc. Biol. 38, 2562–2575. https://doi.org/10.1161/ATVBAHA.118.311185 (2018).
doi: 10.1161/ATVBAHA.118.311185 pubmed: 30354245
Greimel, P. & Ito, Y. First synthesis of natural phosphatidyl-β-D-glucoside. Tetrahedron Lett. 49, 3562–3566. https://doi.org/10.1016/j.tetlet.2008.04.036 (2008).
doi: 10.1016/j.tetlet.2008.04.036
Kano, K. et al. Stereocontrolled synthesis of lyso-phosphatidyl-β-D-Glucoside. ChemistrySelect 6, 6811–6815. https://doi.org/10.1002/slct.202102176 (2021).
doi: 10.1002/slct.202102176
Yamazaki, Y. et al. Comprehensive analysis of monoclonal antibodies against detergent-insoluble membrane/lipid rafts of HL60 cells. J. Immunol. Methods 311, 106–116. https://doi.org/10.1016/j.jim.2006.01.019 (2006).
doi: 10.1016/j.jim.2006.01.019 pubmed: 16564536
Kochiyama, T. et al. Effect of propofol on the production of inflammatory cytokines by human polarized macrophages. Mediators Inflamm. 2019, 1919538. https://doi.org/10.1155/2019/1919538 (2019).
doi: 10.1155/2019/1919538 pubmed: 31007601 pmcid: 6441544

Auteurs

Ryosuke Shimai (R)

Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-Ku, Tokyo, 113-8421, Japan.
Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Tomioka, Urayasu, Chiba, 279-0021, Japan.

Kei Hanafusa (K)

Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Tomioka, Urayasu, Chiba, 279-0021, Japan.

Hitoshi Nakayama (H)

Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Tomioka, Urayasu, Chiba, 279-0021, Japan.
Infection Control Nursing, Juntendo University Graduate School of Health Care and Nursing, 2-5-1 Takasu, Urayasu, Chiba, 279-0021, Japan.

Eriko Oshima (E)

Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Tomioka, Urayasu, Chiba, 279-0021, Japan.

Masaki Kato (M)

Laboratory for Transcriptome Technology, RIKEN Center for Integrative Medical Sciences, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan.

Koki Kano (K)

Division of Molecular Science, Gunma University, Kiryu, Gunma, 376-8515, Japan.

Ichiro Matsuo (I)

Division of Molecular Science, Gunma University, Kiryu, Gunma, 376-8515, Japan.

Tetsuro Miyazaki (T)

Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-Ku, Tokyo, 113-8421, Japan.

Takashi Tokano (T)

Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-Ku, Tokyo, 113-8421, Japan.

Yoshio Hirabayashi (Y)

RIKEN Cluster for Pioneering Research, RIKEN, 2-1, Hirosawa, Wako, Saitama, 351-0198, Japan.

Kazuhisa Iwabuchi (K)

Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Tomioka, Urayasu, Chiba, 279-0021, Japan. iwabuchi@juntendo.ac.jp.
Infection Control Nursing, Juntendo University Graduate School of Health Care and Nursing, 2-5-1 Takasu, Urayasu, Chiba, 279-0021, Japan. iwabuchi@juntendo.ac.jp.
Preparation Office for Establishment of the Faculty of Pharmaceutical Science, Juntendo University, 6-8-1 Hinode , Urayasu, Chiba, 279-0013, Japan. iwabuchi@juntendo.ac.jp.

Tohru Minamino (T)

Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, 2-1-1, Hongo, Bunkyo-Ku, Tokyo, 113-8421, Japan.

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