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Antisense Macrophage Migration Inhibitory Factor (MIF) Prevents Anti‐IgM Mediated Growth Arrest and Apoptosis of a Murine B Cell Line by Regulating Cell Cycle Progression
Author(s) -
Takahashi Akio,
Iwabuchi Kazuya,
Suzuki Masaki,
Ogasawara Kazumasa,
Nishihira Jun,
Onoé Kazunori
Publication year - 1999
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1999.tb02373.x
Subject(s) - macrophage migration inhibitory factor , apoptosis , biology , microbiology and biotechnology , cell cycle , cell growth , cell culture , intracellular , transfection , cell cycle checkpoint , programmed cell death , immunology , cytokine , biochemistry , genetics
Macrophage migration inhibitory factor (MIF) is involved in the generation of cell‐mediated immune responses. Recently it has been reported that MIF also plays a role in cell proliferation and differentiation. In the present study, using a B‐cell line, WEHI‐231, and its stable MIF‐antisense transfectant, WaM2, as a representative transfectant, we investigated the mechanism underlying regulation of the cell growth by MIF. WaM2 cells produced less MIF than vector control or parental WEHI‐231 cells. Reduced and increased proportions were seen in G1 and S‐phase cells, respectively, in WaM2 as compared with WEHI‐231. Growth arrest and apoptosis after stimulation via surface Ig (sIg) were less prominent in WaM2 cells than those in WEHI‐231. However, the addition of recombinant rat MIF did not reverse the inhibition of the growth arrest and apoptosis induced in WaM2 by cross‐linking sIg. Almost the same amount of p27 kipI expression was detected in WaM2 cells as those in WEHI‐231 and vector control cells. Cross‐linking of sIg elevated the p27 kipI level equally in these cells irrespective of the MIF‐antisense expression. Taken together, it seems that MIF plays a role in inducing apoptosis in B cells upon IgM cross‐linking by regulating the cell cycle via a novel intracellular pathway.