Cited by 30T-cell and B-cell ImmunologyProtein Tyrosine PhosphatasesCell death mechanisms and regulation

Protein phosphatase subunit G5PR is needed for inhibition of B cell receptor-induced apoptosis

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Xing, Yan, Igarashi, Hideya, Wang, Xiaodan, Sakaguchi, Nobuo·2005·The Journal of Experimental Medicine

Abstract

B cell receptor (BCR) cross-linking induces B cell proliferation and sustains survival through the phosphorylation-dependent signals. We report that a loss of the protein phosphatase component G5PR increased the activation-induced cell death (AICD) and thus impaired B cell survival. G5PR associates with GANP, whose expression is up-regulated in mature B cells of the peripheral lymphoid organs. To study G5PR function, the G5pr gene was conditionally targeted with the CD19-Cre combination (G5pr(-/-) mice). The G5pr(-/-) mice had a decreased number of splenic B cells (60% of the controls). G5pr(-/-) B cells showed a normal proliferative response to lipopolysaccharide or anti-CD40 antibody stimulation but not to BCR cross-linking with or without IL-4 in vitro. G5pr(-/-) B cells did not show abnormalities in the BCR-mediated activation of Erks and NF-kappaB, cyclin D2 induction, or Akt activation. However, G5pr(-/-) B cells were sensitive to AICD caused by BCR cross-linking. This was associated with an increased depolarization of the mitochondrial membrane and the enhanced activation of c-Jun NH(2)-terminal protein kinase and Bim. These results suggest that G5PR is required for the BCR-mediated proliferation associated with the prevention of AICD in mature B cells.

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  • These results imply the existence of a G5PR-dependent resistance mechanism to BCR-activation-induced apoptosis in mature B-cells.

    “These results imply the existence of a G5PRdependent resistance mechanism to BCR-activation-induced apoptosis in mature B-cells [76]”
  • G5PR knockout cells showed prolonged Bim phosphorylation after BCR cross-linking, accompanied by sustained JNK activation and enhanced mitochondrial membrane depolarization.

    “Upon analysis, cells showed prolonged Bim phosphorylation after BCR cross-linking, accompanied by sustained JNK activation and enhanced mitochondrial membrane depolarization.”
  • In contrast to G5PR-deficient B-cells, apoptosis in G5PR-deficient thymocytes seemed caspase-3 dependent and Bim-independent.

    “in contrast to the mechanism in G5PR-deficient B-cells [76], apoptosis seemed to be caspase-3 dependent and Bim-independent.”
  • The reduced number of mature B-cells in B-cell-specific B′′γ/G5PR knockout mice was attributed to impaired B-cell survival and increased BCR-activation-induced apoptosis, rather than to a proliferation defect.

    “the reduced number of mature B-cells in spleen, lymph nodes and peripheral blood that was seen in a B-cell specific KO of B″γ/G5PR (Ppp2r3c), was attributed to impaired B-cell survival and increased BCR-activation-induced apoptosis, rather than to a proliferation defect [76].”
  • Transgenic overexpression of G5PR in lymphoid cells achieved a 4.5-times overexpression in isolated splenocytes.

    “in which a 4.5-times overexpression of G5PR was confirmed in isolated splenocytes.”

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Authors
Xing, Y., Igarashi, H., Wang, X., & Sakaguchi, N.
Affiliations
Japan Science and Technology Agency (JP)
Venue
The Journal of Experimental Medicine
Published
2005-08-29
Volume
202
Issue
5
Pages
707-719
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2142184914
Cited by
30
References
74
Citations by year
2025: 1 · 2024: 6 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 1 · 2018: 2 · 2016: 2 · 2015: 2 · 2013: 1 · 2012: 1
FWCI
0.71
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
protein phosphatase, B cell receptor signaling, activation-induced cell death, B cell survival, GANP, B cell proliferation, mitochondrial depolarization, JNK, building information modeling, NF-κB, Akt, ERK, cyclin D2
MeSH terms
Bcl-2-Like Protein 11, Animals, B-Lymphocytes, Flow Cytometry, Membrane Proteins, Nuclear Proteins, Phosphoprotein Phosphatases, Phosphoproteins, Proto-Oncogene Proteins, Receptors, Antigen, B-Cell, Blotting, Western, Apoptosis, DNA Primers, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, In Situ Nick-End Labeling, Gene Silencing, Protein Subunits, JNK Mitogen-Activated Protein Kinases, Apoptosis Regulatory Proteins, Mitochondrial Membranes, Mice

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