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Involvement of RhoA/ROCK signaling for alteration of stress fiber via lymphotoxin β receptor stimulation in fibroblastic reticular cell isolated from lymph node

Animal Cells and Systems 2013년 17권 6호 p.421 ~ 428
이재설, 김연희, 이종환,
소속 상세정보
이재설 ( Lee Jae-Seol ) - Dong-Eui University Department of Biomaterial Control
김연희 ( Kim Yeon-Hee ) - Pusan National University Department of Biology Education
이종환 ( Lee Jong-Hwan ) - Dong-Eui University Department of Biomaterial Control

Abstract


The heterotrimeric transmembrane lymphotoxin α1β2 (LTα1β2), member of the tumor necrosis factor family cytokines including soluble homotrimeric lymphotoxin α (LTα), plays an important role in lymphoid tissue architecture and organogenesis. We found that lymphotoxin β receptor (LTβR) stimulation using agonistic anti-LTβR antibody induced the changes in actin stress fiber and morphology of cells. To address the possibility that LTβR stimulation is involved in RhoA/Rho-associated protein kinase (ROCK) signaling, we checked the level of Rho-guanosine diphosphate (GDP)/guanosine triphosphate (GTP) exchange activity with fibroblastic reticular cell (FRC) lysate. When LTβR was stimulated with agonistic anti-LTβR antibody, the Rho-GDP/GTP exchange activity was markedly reduced. Inhibition of ROCK activity induced changes in actin cytoskeleton organization and cell morphology in FRC. We showed that the phosphorylation of myosin light chains (MLCs) was reduced by LTβR stimulation in FRC. DNA gene chip demonstrated that agonistic anti-LTβR antibody in FRC affected the downregulation of actin filament and myosin component transcripts. The results provided here indicated that RhoA/ROCK was responsible for the observed phosphorylation of MLC. Collectively, these results suggest that LTβR stimulation is involved in change of stress fiber via RhoA/ROCK signaling in FRC.

키워드

FRC; LTβR; p-MLC; RhoA/ROCK; stress fiber

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