ArticleInternational journal of molecular medicine2017
MAPK/p38 regulation of cytoskeleton rearrangement accelerates induction of macrophage activation by TLR4, but not TLR3.
Article in International journal of molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
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- Characterization of Breast Cancer Aggressiveness by Cell Mechanics.International journal of molecular sciences · 2023Article
- Osmotically Rupturing Phagosomes in Macrophages Using PNIPAM Microparticles.ACS applied materials & interfaces · 2023Article
- RCAS1 increases cell morphological changes in murine fibroblasts by reducing p38 phosphorylation.Molecular medicine reports · 2023Article
- MRTF may be the missing link in a multiscale mechanobiology approach toward macrophage dysfunction in space.Frontiers in cell and developmental biology · 2022Article
- HBeAg mediates inflammatory functions of macrophages by TLR2 contributing to hepatic fibrosis.BMC medicine · 2021Article
- Negative feedback loop of ERK/CREB/miR-212-3p inhibits HBeAg-induced macrophage activation.Journal of cellular and molecular medicine · 2020Article
- HBeAg induces the expression of macrophage miR-155 to accelerate liver injury via promoting production of inflammatory cytokines.Cellular and molecular life sciences : CMLS · 2018Article
- The E3 ubiquitin ligase MuRF2 attenuates LPS-induced macrophage activation by inhibiting production of inflammatory cytokines and migration.FEBS open bio · 2018Article
- Role of inflammatory response in liver diseases: Therapeutic strategies.World journal of hepatology · 2018Review
- Glucomannan is a promising isoniazid's enhancer that inducing macrophage phagocytosis.Journal of advanced pharmaceutical technology & researchArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptor 3 (TLR3) and TLR4 utilize adaptor proteins to activate mitogen‑activated protein kinase (MAPK), resulting in the acute but transient inflammatory response aimed at the clearance of pathogens. In the present study, it was demonstrated that macrophage activation by lipopolysaccharide (LPS) or poly(I:C), leading to changes in cell morphology, differed significantly between the mouse macrophage cell line RAW264.7 and mouse primary peritoneal macrophages. Moreover, the expression of α- and β-tubulin was markedly decreased following LPS stimulation. By contrast, α- and β-tubulin expression were only mildly increased following poly(I:C) treatment. However, the expression of β-actin and GAPDH was not significantly affected. Furthermore, it was verified that vincristine pretreatment abrogated the cytoskeleton rearrangement and decreased the synthesis and secretion of proinflammatory cytokines and migration of macrophages caused by LPS. Finally, it was observed that the MAPK/p38 signaling pathway regulating cytoskeleton rearrangement may participate in LPS‑induced macrophage cytokine production and migration. Overall, the findings of the present study indicated that MAPK/p38 regulation of the cytoskeleton, particularly tubulin proteins, plays an important role in LPS-induced inflammatory responses via alleviating the synthesis and secretion of proinflammatory cytokines and inhibiting the migration of macrophages.
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