VEGFR1 Signaling Regulates IL-4-Mediated Arginase 1 Expression in Macrophages
| Autor: | Qishan Chen, Rong Ju, Zhimin Ye, Xifang Li, Y Zou |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
animal structures
Mice Transgenic Biochemistry Gene Expression Regulation Enzymologic Mice 0404 agricultural biotechnology Immune system Western blot 0502 economics and business medicine Macrophage Animals Molecular Biology Interleukin 4 Innate immune system Vascular Endothelial Growth Factor Receptor-1 medicine.diagnostic_test Arginase Chemistry Macrophages 05 social sciences 04 agricultural and veterinary sciences General Medicine 040401 food science Immunity Innate Cell biology body regions PIGF cardiovascular system Molecular Medicine 050211 marketing Interleukin-4 Tyrosine kinase Gene Deletion Signal Transduction |
| Zdroj: | Current molecular medicine. 17(4) |
| ISSN: | 1875-5666 |
| Popis: | Background Macrophages undergo polarization or activation in response to environmental stimuli, an essential process for proper immune response. Meanwhile, excessive activation of macrophages causes autoimmune diseases. It is therefore crucial to prevent over-activation of macrophage in order to maintain the proper immune response. Arginase 1 (Arg-1) plays a critical role in coordinating the immune response by regulating availability of arginine. Objective To understand the mechanism of Arg-1 regulation. Methods Real-time PCR and Western Blot analysis were utilized to examine the Arg-1 levels expressed from the VEGFR1-deleted and VEGFR1-TK-deficient bone marrowderived macrophages (BMDMs). Results The VEGFR1-mediated signaling suppressed IL-4-induced Arg-1 expression. Deletion of VEGFR1 resulted in elevated Arg-1 expression and the tyrosine kinase domain of VEGFR1 was required for the suppression. Each of three ligands of VEGFR1, VEGF-A, VEGF-B and PIGF, mediated the inhibition to the similar degree. Conclusion Our findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 potentially to maintain the proper innate immune response. |
| Databáze: | OpenAIRE |
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