ArticleAmerican journal of physiology. Cell physiology2019
A distinct transcriptional profile in response to endothelial monocyte activating polypeptide II is partially mediated by JAK-STAT3 in murine macrophages.
Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The redundant protein synthesis gene Aimp1 challenges the canonical inverse relationship between translation and autophagy.Communications biology · 2026Article
- Roles of Lipid Metabolism in Pulmonary Hypertension: Friend or Foe?Biomolecules · 2025Review
- Peripheral Blood-Derived Mesenchymal Stem Cells Modulate Macrophage Plasticity through the IL-10/STAT3 Pathway.Stem cells international · 2022Article
- SUMOylation of Arginyl tRNA Synthetase Modulates theFrontiers in cell and developmental biology · 2021Article
- Mechanistic regulation of SPHK1 expression and translocation by EMAP II in pulmonary smooth muscle cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Article
- Roles of aminoacyl-tRNA synthetase-interacting multi-functional proteins in physiology and cancer.Cell death & disease · 2020Review
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Macrophages are important responders to environmental changes such as secreted factors. Among the secreted factors in injured tissues, the highly conserved endothelial monocyte activating polypeptide II (EMAP II) has been characterized to limit vessel formation, to be locally expressed near sites of injury labeling it a "find-me" signal, and to recruit macrophages and neutrophils. The molecular mechanisms mediated by EMAP II within macrophages once they are recruited are unknown. In this study, using a model of partially activated, recruited thioglycollate-elicited peritoneal macrophages, a transient, transcription profile of key functional genes in macrophages exposed to EMAP II was characterized. We found that EMAP II-mediated changes were elicited mainly through signal transducer and activator of transcription 3 (STAT3) as evidenced by increased Y705 phosphorylation and changes in activity and upstream of it, Janus associated kinase (JAK)1/2 upstream. Both inhibition of JAK1/2 and knockdown of Stat3 abrogated a subset of genes that are upregulated by EMAP II. Our results identify a rapid EMAP II-mediated STAT3 activation that coincides with altered pro- and anti-inflammatory gene expression in macrophages.
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