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KMID : 0613820190290020256
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Journal of Life Science
2019 Volume.29 No. 2 p.256 ~ p.264
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Signals of MLCK and ROCK Pathways Triggered via Lymphotoxin β Receptor are Involved in Stress Fiber Change of Fibroblastic Reticular Cells
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Kim Dae-Sik
Lee Jong-Hwan
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Abstract
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Lymphotoxin β receptor (LTβR), a member of the tumor necrosis factor receptor family, plays an important role in lymphoid tissue’s architecture and organogenesis. In contrast, MLCK and ROCK play critical roles in the regulation of stress fiber (SF) formation in cells. To determine whether LTβR stimulation in fibroblastic reticular cells (FRCs) is involved in these signaling pathways, myosin light chain kinase inhibitor-7 (ML-7) was used to inhibit them. ML7-treated FRCs completely blocked SFs and showed retraction and shrinkage processes comparable to those observed in agonistic anti-LTβR antibody-treated cells. The inhibition of ROCK activity with Y27632-induced changes in actin cytoskeleton organization and cell morphology in FRCs. Actin bundles rearranged into SFs, and phospho-myosin light chain (p-MLC) co-localized in FRCs. We checked the level of Rho-guanosine diphosphate (Rho- GDP)/guanosine triphosphate (GTP) exchange activity using FRC lysate. When LTβR was stimulated with agonistic anti-LTβR antibodies, Rho-GDP/GTP exchange activity was markedly reduced. Regarding LTβR signaling with a focus on MLCK inhibition, we showed that the phosphorylation of MLCs was reduced by LTβR stimulation in FRCs. Cytoskeleton components, such as tubulin, b-actin, and phospho-ezrin proteins acting as membrane-cytoskeleton linkers, were produced in de-phosphorylation, and they reduced expression in agonistic anti-LTβR antibody-treated FRCs. Collectively, the results suggested that MLCK and ROCK were simultaneously responsible for SF regulation triggered by LTβR signaling in FRCs.
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KEYWORD
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FRC (Fibroblastic reticular cell), LTβR (Lymphotoxin β receptor), MLCK, ROCK, SF (stress fiber)
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