5 years ago

An Essential Role for TAGLN2 in Phagocytosis of Lipopolysaccharide-activated Macrophages

Kyung-Sik Lee, Hyun-Su Lee, Hye-Ran Kim, In Duk Jung, Sang-Myeong Lee, Myung-Han Yoon, Seong-Min Kim, Chang-Hyun Kim, Min-Sung Kwon, Chang-Duk Jun, Yeong-Min Park
Activated macrophages have a greater ability of phagocytosis against pathogens that is mediated by large-scale actin rearrangement. However, molecular machineries that conduct this task have not been fully identified. Here, we demonstrate an unanticipated role of TAGLN2, a 22-kDa actin-binding protein, in Toll-like receptor (TLR)-stimulated phagocytosis. TAGLN2 was greatly induced in macrophages in response to lipopolysaccharide (LPS), a ligand for TLR4, partly via the NF-κB pathway. TAGLN2-deficient macrophages (TAGLN2−/−) showed defective phagocytic functions of IgM- and IgG-coated sheep red blood cells as well as bacteria. Cell signaling pathways involved in actin rearrangement—PI3 kinase/AKT and Ras-ERK—were also down-regulated in LPS-stimulated TAGLN2-deficient macrophages. Moreover, TAGLN2−/− mice showed higher mortality after bacterial infection than wild-type littermates. Thus, our results revealed a novel function of TAGLN2 as a molecular armament required for host defense.

Publisher URL: https://www.nature.com/articles/s41598-017-09144-x

DOI: 10.1038/s41598-017-09144-x

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