Increased p190RhoGEF expression in activated B cells correlates with the induction of the plasma cell differentiation.
10.3858/emm.2012.44.2.009
- Author:
Yun Jung HA
1
;
Ji Hye JEONG
;
Yuna PARK
;
Jong Ran LEE
Author Information
1. Division of Life and Pharmaceutical Sciences, College of Natural Sciences, Ewha Womans University, Seoul 120-750, Korea. jrlee@ewha.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
antigens, CD40;
ARHGAP35 protein, human;
B-lymphocytes;
CD40;
cell differentiation;
p190RhoGEF;
plasma cells;
rhoA GTP-binding protein
- MeSH:
Animals;
B-Lymphocytes/*cytology/*metabolism;
Cell Differentiation/genetics/*physiology;
Cell Line;
Cells, Cultured;
Female;
Guanine Nucleotide Exchange Factors/genetics/*metabolism;
Humans;
Lymphocyte Activation/genetics/*physiology;
Mice;
Mice, Inbred BALB C;
Plasma Cells/*cytology/*metabolism;
rhoA GTP-Binding Protein/genetics/metabolism
- From:Experimental & Molecular Medicine
2012;44(2):138-148
- CountryRepublic of Korea
- Language:English
-
Abstract:
Previously, we demonstrated that the p190 Rho guanine nucleotide exchange factor (p190RhoGEF) was induced following CD40 stimulation of B cells. In this study, we examined whether p190RhoGEF and a downstream effector molecule RhoA are required for B cell differentiation. Expression of p190RhoGEF positively correlated with the expression of surface markers and transcriptional regulators that are characteristic of mature B cells with plasma cell (PC) phenotypes. Moreover, either the overexpression of p190RhoGEF or the expression of a constitutively active RhoA drove cellular differentiation toward PC phenotypes. B cell maturation was abrogated in cells that overexpressed p190RhoGEF and a dominant-negative form of RhoA simultaneously. CD40-mediated maturation events were also abrogated in cells that overexpressed either dominant-negative p190RhoGEF or RhoA. Together, these data provide evidence that p190RhoGEF signaling through RhoA in CD40-activated B cells drives the induction of the PC differentiation.
