scholarly journals Thy28 partially prevents apoptosis induction following engagement of membrane immunoglobulin in WEHI-231 B lymphoma cells

2012 ◽  
Vol 17 (1) ◽  
Author(s):  
Hiroko Toyota ◽  
Xiao-Zhou Jiang ◽  
Hideki Asakura ◽  
Junichiro Mizuguchi
Keyword(s):  
Mammalian Cells ◽  
Late Phase ◽  
G1 Phase ◽  
H2o2 Production ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Histocompatibility Complex ◽  
Membrane Immunoglobulin ◽  
B Lymphoma Cells ◽  
Wehi 231

AbstractThy28 protein is conserved among plants, bacteria, and mammalian cells. Nuclear Thy28 protein is substantially expressed in testis, liver, and immune cells such as lymphocytes. Lymphocyte apoptosis plays a crucial role in homeostasis and formation of a diverse lymphocyte repertoire. In this study, we examined whether Thy28 affects induction of apoptosis in WEHI-231 B lymphoma cells following engagement of membrane immunoglobulin (mIg). Once they were established, the Thy28-overexpressing WEHI-231 cells showed similar expression levels of IgM and class I major histocompatibility complex (MHC) molecule compared with controls. The Thy28-overexpressing cells were considerably resistant to loss of mitochondrial membrane potential (ΔΨm), caspase-3 activation, and increase in annexin-positive cells upon mIg engagement. These changes were concomitant with an increase in G1 phase associated with upregulation of p27Kip1. The anti-IgM-induced sustained activation of c-Jun N-terminal kinase (JNK), which was associated with late-phase hydrogen peroxide (H2O2) production, was partially reduced in the Thy28-expressing cells relative to controls. Taken together, the data suggest that in WEHI-231 B lymphoma cells, Thy28 regulates mIg-mediated apoptotic events through the JNK-H2O2 activation pathway, concomitant with an accumulation of cells in G1 phase associated with upregulation of p27Kip1 in WEHI-231 B lymphoma cells.

The role of bcl-xL in CD40-mediated rescue from anti-μ-induced apoptosis in WEHI-231 B lymphoma cells

1995 ◽  
Vol 25 (5) ◽  
pp. 1352-1357 ◽  
Author(s):  
Michael S. K. Choi ◽  
Lawrence H. Boise ◽  
Alexander R. Gottschalk ◽  
José Quintans ◽  
Craig B. Thompson ◽  
...  
Keyword(s):  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
Induced Apoptosis

scholarly journals Roles of the Tumor Suppressor p53 and the Cyclin-dependent Kinase Inhibitor p21WAF1/CIP1 in Receptor-mediated Apoptosis of WEHI 231 B Lymphoma Cells

1998 ◽  
Vol 187 (10) ◽  
pp. 1671-1679 ◽  
Author(s):  
Min Wu ◽  
Robert E. Bellas ◽  
Jian Shen ◽  
Gail E. Sonenshein
Keyword(s):  
Tumor Suppressor ◽  
B Cell ◽  
Kinase Inhibitor ◽  
Ectopic Expression ◽  
Cyclin Dependent Kinase ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Cyclin Dependent Kinase Inhibitor ◽  
B Lymphoma Cells ◽  
Wehi 231

Treatment of WEHI 231 immature B lymphoma cells with an antibody against their surface immunoglobulin M (anti-IgM) induces apoptosis and has been studied extensively as a model of self-induced B cell tolerance. Since the tumor suppressor protein p53 has been implicated in apoptosis in a large number of cell types and has been found to be mutated in a variety of B cell tumors, here we sought to determine whether p53 and the p53 target gene cyclin-dependent kinase inhibitor p21WAF1/CIP1 were involved in anti-IgM–induced cell death. Anti-IgM treatment of WEHI 231 cells increased expression of p53 and p21 protein levels. Ectopic expression of wild-type p53 in WEHI 231 cells induced both p21 expression and apoptosis. Ectopic expression of p21 similarly induced apoptosis. Rescue of WEHI 231 cells from apoptosis by costimulation with CD40 ligand ablated the increase in p21 expression. Lastly, a significant decrease in anti-IgM–mediated apoptosis was seen upon downregulation of endogenous p53 activity by expression of a dominant-negative p53 protein or upon microinjection of an antisense p21 expression vector or antibody. Taken together, the above data demonstrate important roles for p53 and p21 proteins in receptor-mediated apoptosis of WEHI 231 B cells.

scholarly journals c-Jun N-terminal kinase (JNK) is required for survival and proliferation of B-lymphoma cells

Blood ◽  
2005 ◽  
Vol 106 (4) ◽  
pp. 1382-1391 ◽  
Author(s):  
Murali Gururajan ◽  
Roger Chui ◽  
Anbu K. Karuppannan ◽  
Jiyuan Ke ◽  
C. Darrell Jennings ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
Dependent Manner ◽  
Lymphoma Cells ◽  
Cd40 Ligation ◽  
B Lymphoma ◽  
Protein Levels ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
M Phase ◽  
Mitogen Activated Protein

AbstractSeveral primary murine and human B lymphomas and cell lines were found to constitutively express high levels of the activated form of c-jun N-terminal kinase (JNK), a member of the mitogen-activated protein (MAP) kinase family. Proliferation of murine B lymphomas CH31, CH12.Lx, BKS-2, and WEHI-231 and the human B lymphomas BJAB, RAMOS, RAJI, OCI-Ly7, and OCI-Ly10 was strongly inhibited by SP600125, an anthrapyrazolone inhibitor of JNK, in a dose-dependent manner. The lymphoma cells underwent apoptosis and arrested at the G2/M phase of cell cycle. Furthermore, JNK-specific small interfering RNA (siRNA) inhibited the growth of both murine and human B lymphomas. Thus in the B-lymphoma model, JNK appears to have a unique prosurvival role. Survival signals provided by CD40 and interleukin-10 (IL-10) together reversed the growth inhibition induced by the JNK inhibitor. c-Myc protein levels were reduced in the presence of both SP600125 and JNK-specific siRNA, and CD40 ligation restored c-Myc levels. Moreover, Bcl-xL rescued WEHI-231 cells from apoptosis induced by the JNK inhibitor. The JNK inhibitor also reduced levels of early growth response gene-1 (Egr-1) protein, and overexpressing Egr-1 partially rescued lymphoma cells from apoptosis. Thus, JNK may act via c-Myc and Egr-1, which were shown to be important for B-lymphoma survival and growth. (Blood. 2005;106:1382-1391)

Increased degradation of protein kinase C without diminution of mRNA level after treatment of WEHI-231 B lymphoma cells with phorbol esters

1988 ◽  
Vol 155 (3) ◽  
pp. 1311-1317 ◽  
Author(s):  
Junichiro Mizuguchi ◽  
Hiroki Nakabayashi ◽  
Yasuyoshi Yoshida ◽  
Kuo-Ping Huang ◽  
Tetsuya Uchida ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phorbol Esters ◽  
Mrna Level ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
Kinase C ◽  
B Lymphoma Cells ◽  
Wehi 231

Transient down-regulation of PKC-ζ RNA following crosslinking of membrane IgM on WEHI-231 B lymphoma cells

1992 ◽  
Vol 142 (2) ◽  
pp. 303-312 ◽  
Author(s):  
Akito Tsutsumi ◽  
Jose Freire-Moar ◽  
John T. Ransom
Keyword(s):  
Lymphoma Cells ◽  
Down Regulation ◽  
B Lymphoma ◽  
B Lymphoma Cells ◽  
Wehi 231 ◽  
Pkc Ζ

B cell receptor-induced growth arrest and apoptosis in WEHI-231 immature B lymphoma cells involve cyclic AMP and Epac proteins

2009 ◽  
Vol 21 (4) ◽  
pp. 609-621 ◽  
Author(s):  
Maria Grandoch ◽  
Maider López de Jesús ◽  
Paschal A. Oude Weernink ◽  
Artur-Aron Weber ◽  
Karl H. Jakobs ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
B Cell ◽  
Growth Arrest ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Lymphoma Cells ◽  
B Lymphoma ◽  
B Lymphoma Cells ◽  
Wehi 231
Sign in / Sign up

Export Citation Format

Share Document