The roles of a ribosomal protein S19 polymer in a mouse model of carrageenan-induced acute pleurisy

Yamanegi, Koji; Kawakami, Toru; Yamada, Naoko; Kumanishi, Shunsuke; Futani, Hiroyuki; Nakasho, Keiji; Nishiura, Hiroshi

doi:10.1016/j.imbio.2017.02.001

Cited by 7 publications

(5 citation statements)

References 48 publications

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“…Recently, we prepared Gln137Glu RP S19 mutant knock‐in C57BL/6J mice (knock‐in mice) and made a carrageenan‐induced acute pleurisy mouse model . In this case, neutrophils were still present in the thoracic cavities of the knock‐in mice at 24 h after carrageenan injection.…”

Section: Discussionmentioning

confidence: 99%

“…The GTPase activity of RGS3 inhibits G protein‐dependent downstream signaling . Therefore, we suggested that the interaction of C5aR with RP S19 polymer decreases the neutrophil cell lifespan during the resolution phase …”

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confidence: 99%

“…11 Therefore, we suggested that the interaction of C5aR with RP S19 polymer decreases the neutrophil cell lifespan during the resolution phase. 12 Conversely, LDR binds to the macrophage C5aR, and IAGQVAAANKKH also interacts with the macrophagespecific calcium-dependent phospholipid-binding protein annexin A3 (ANXA3). 13 ANXA3 seems to enhance the C5aRmediated p38 mitogen-activated protein kinase (p38MAPK) signal.…”

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confidence: 99%

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Participation of delta annexin A3 in the ribosomal protein S19 C‐terminus‐dependent inhibitory mechanism of the neutrophil C5a receptor through delta lactoferrin

Yamanegi

Yamada²,

Nakasho³

et al. 2017

Pathology International

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Although C5a receptor (C5aR) interacting with its agonist C5a promotes acute inflammation during the initiation phase, the roles of the recycling C5aR during the resolution phase are still unclear. We found that C5aR interacted with its antagonist/agonist ribosomal protein S19 (RP S19) polymer or a RP S19 polymer functional analogue S-tagged C5a/RP S19, which connects an RP S19 C-terminus (IAGQVAAANKKH) to the S-tagged C5a C-terminus, promoted acute inflammation at the resolution phase via an activation of the apoptosis-inducing transcription factor delta lactoferrin (δLf) in neutrophils and the membrane mobilizing factor full-length annexin A3 (ANXA3) in macrophages. To confirm the antagonistic system of the recycling C5aR, S-tagged δLf-coupled BrCN-activated Sepharose 4B beads were incubated with cytoplasmic proteins and identified a neutrophil-specific δANXA3 via pull-down experiments. The S-tagged C5a/RP S19-induced agonistic functions in macrophage-like cells that were differentiated from human promyelocytic leukemia HL-60 cells by phorbol-12-myristate-13-acetate were suppressed by δLf and δANXA3 co-overexpression. δANXA3 seems to participate in the antagonistic system of the neutrophil C5aR involving IAGQVAAANKKH and δLf. Most likely, δANXA3 works as antagonist for the recycling C5aR on neutrophils during the resolution phase of acute inflammation.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Participation of delta annexin A3 in the ribosomal protein S19 C‐terminus‐dependent inhibitory mechanism of the neutrophil C5a receptor through delta lactoferrin

Yamanegi

Yamada²,

Nakasho³

et al. 2017

Pathology International

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“…However, the Q137E mutant RP S19 polymer with alternative cross-linkages did not attract blood monocytes/macrophages. To validate this hypothesis, Q137E mutant RP S19 gene knock-in C57BL/6J mice (KI mice) were prepared ( Yamanegi et al, 2017 ). In contrast to the number of white blood cells (WBCs) in peripheral blood cells in 12-week-old control C57BL/6J mice (WT mice), the number of WBCs slightly decreased in 24-week-old WT mice.…”

Section: Roles Of Senescent Macrophages In Ki Mice In the Experimental Shift From Acute Inflammation To Chronic Inflammationmentioning

confidence: 99%

Immune Aging and How It Works for Inflammation and Fibrosis

et al. 2022

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Almost all mature cells that undergo apoptosis in an age-dependent or an accidental manner are completely recovered in tissue-specific microenvironments without any physiological changes. After peripheral blood leukocytes are released into the local region, fibroblast cells and new blood vessels commonly proliferate during wound healing. Inducible repair tools mainly supplied from blood vessels are cleared by peripheral blood phagocytic macrophages. Finally, hematopoietic stem cell (HSC)-derived precursor cells migrate from bone marrow (BM) to the microenvironment to rebuild damaged tissues (the mature immune system). In contrast to the mature immune system, the effects of aging on HSCs (long-term HSCs) and peripheral blood lymphocytes (long-term PBLs) are not clearly understood in the BM and thymus niches with tissue-specific microenvironments with some physiological changes (the aged BM niche) for incomplete rebuilding of damaged tissues (the aged immune system). In this review, the roles of the aged immune system in both a delay of acute inflammation and the development of chronic inflammation or fibrosis are discussed.

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“…In addition, it was also shown that the ribosomal protein S19 (RP S19) polymer cross-linked at Lys122 and Gln137 by transglutaminases released from apoptotic neutrophils acts as a C5aR ligand during the resolution phase of acute inflammation. In the absence of TG2 activity the resolution was also found to be delayed in the carrageenan-induced acute pleurisy in C57BL/6J model mice [ 150 ].…”

Section: Transglutaminase 2 and Other Inflammatory Diseasesmentioning

confidence: 99%

Transglutaminase 2 in human diseases

Szondy¹,

Korponay-Szabó²,

Király³

et al. 2017

BioMedicine

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Transglutaminase 2 (TG2) is an inducible transamidating acyltransferase that catalyzes Ca(2+)-dependent protein modifications. In addition to being an enzyme, TG2 also serves as a G protein for several seven transmembrane receptors and acts as a co-receptor for integrin β1 and β3 integrins distinguishing it from other members of the transglutaminase family. TG2 is ubiquitously expressed in almost all cell types and all cell compartments, and is also present on the cell surface and gets secreted to the extracellular matrix via non-classical mechanisms. TG2 has been associated with various human diseases including inflammation, cancer, fibrosis, cardiovascular disease, neurodegenerative diseases, celiac disease in which it plays either a protective role, or contributes to the pathogenesis. Thus modulating the biological activities of TG2 in these diseases will have a therapeutic value.

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The roles of a ribosomal protein S19 polymer in a mouse model of carrageenan-induced acute pleurisy

Cited by 7 publications

References 48 publications

Participation of delta annexin A3 in the ribosomal protein S19 C‐terminus‐dependent inhibitory mechanism of the neutrophil C5a receptor through delta lactoferrin

Participation of delta annexin A3 in the ribosomal protein S19 C‐terminus‐dependent inhibitory mechanism of the neutrophil C5a receptor through delta lactoferrin

Immune Aging and How It Works for Inflammation and Fibrosis

Transglutaminase 2 in human diseases

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