Interleukin-19 induces angiogenesis in the absence of hypoxia by direct and indirect immune mechanisms

Kako, Farah; Gabunia, Khatuna; Ray, Mitali; Kelemen, Sheri E.; England, Ross N.; Kako, Bashar; Scalia, Rosario; Autieri, Michael V.

doi:10.1152/ajpcell.00006.2016

Cited by 28 publications

(26 citation statements)

References 46 publications

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“…Furthermore, Th17 and Th2 cytokines, including IL-17A, IL-4 and IL-13, induce IL-19 expression in airway epithelial cells [15], where it may be involved in asthma and tissue fibrosis as part of a complex cellular interactions between Th17 cells, Th2 cells and airway epithelial cells. IL-19 is also involved in tissue injury and inflammation, as it induces angiogenesis by promoting proangiogenic genes expression in both endothelial cells and macrophages [31, 32]. …”

Section: Immunobiology Of the Il-20r Cytokinesmentioning

confidence: 99%

IL-20 receptor cytokines in autoimmune diseases

Chen

Caspi

Chong

2018

Journal of Leukocyte Biology

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IL-19, IL-20, and IL-24 are the members of IL-10 family. They are also known as IL-20 receptor (IL-20R) cytokines as they all signal through the IL-20RA/IL-20RB receptor complex; IL-20 and IL-24 (but not IL-19) also signal through the IL-20RB/IL22RA1 receptor complex. Despite their protein structure homology and shared use of receptor complexes, they display distinct biological functions in immune regulation, tissue homeostasis, host defense, and oncogenesis. IL-20R cytokines can be expressed by both immune cells and epithelial cells, and are important for their interaction. In general, these cytokines are considered to be associated with pathogenesis of chronic inflammation and autoimmune diseases, including psoriasis, rheumatoid arthritis, and inflammatory bowel disease. However, a number of studies also highlighted their suppressive functions in regulating both innate and adaptive T cell responses and other immune cells, suggesting that the role of IL-20R cytokines in autoimmunity may be complex. In this review, we will discuss the immunobiological functions of IL-20R cytokines and how they are involved in regulating autoimmune diseases.

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Section: Immunobiology Of the Il-20r Cytokinesmentioning

confidence: 99%

IL-20 receptor cytokines in autoimmune diseases

Chen

Caspi

Chong

2018

Journal of Leukocyte Biology

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“…Il19 2/2 mice have impaired neovascularization during recovery from murine hindlimb ischemia, which could be rescued by subcutaneous injection of rmIL-19 (6). More recently, we reported that IL-19 could induce angiogenesis in normoxic conditions (7).…”

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confidence: 93%

RNA stability protein ILF3 mediates cytokine‐induced angiogenesis

et al. 2018

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Interleukin enhancer‐binding factor 3 (ILF3), an RNA‐binding protein, is best known for its role in innate immunity by participation in cellular antiviral responses. A role for ILF3 in angiogenesis is unreported. ILF3 expression in CD31+ capillaries of hypoxic cardiac tissue was detected by immunohistochemistry. Proangiogenic stimuli induce ILF3 mRNA and protein expression in cultured human coronary artery endothelial cells (hCAECs). Angiogenic indices, including proliferation, migration, and tube formation, are all significantly reduced in hCAECs when ILF3 is knocked down using small interfering RNA (siRNA), but are significantly increased when ILF3 is overexpressed using adenovirus. Protein and mRNA abundance of several angiogenic factors including CXCL1, VEGF, and IL‐8 are decreased when ILF3 is knocked down by siRNA. These factors are increased when ILF3 is overexpressed by adenovirus. ILF3 is phosphorylated and translocates from the nucleus to the cytoplasm in response to angiogenic stimuli. Proangiogenic transcripts containing adenine and uridine‐rich elements were bound to ILF3 through RNA immunoprecipitation. ILF3 stabilizes proangiogenic transcripts including VEGF, CXCL1, and IL‐8 in hCAECs. Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis. Our working hypothesis is that ILF3 promotes angiogenesis through cytokine‐inducible mRNA stabilization of proangiogenic transcripts.—Vrakas, C. N., Herman, A. B., Ray, M., Kelemen, S. E., Scalia, R., Autieri, M. V. RNA stability protein ILF3 mediates cytokine‐induced angiogenesis. FASEB J. 33, 3304–3316 (2019). http://www.fasebj.org

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“…In our experiments , IL‐19 treatment enhanced protein expression of VEGF in myocardium of mice with MI. An in vivo assay reported that IL‐19(−/−) mice responded to VEGF significantly less than wild‐type mice and demonstrated decreased capillary formation in Matrigel plugs (Kako et al ., ), indicating that IL‐19‐induced angiogenesis was not only dependent on its up‐regulation of VEGF. Macrophages polarized toward an M2 phenotype had a higher angiogenic potential, compared with other macrophage subsets (Zajac et al ., ; Jetten et al ., ).…”

Section: Discussionmentioning

confidence: 96%

Exogenous IL‐19 attenuates acute ischaemic injury and improves survival in male mice with myocardial infarction

Zhang

et al. 2019

British J Pharmacology

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Background and purpose Myocardial infarction (MI) is one of the leading causes of death in China and often results in the development of heart failure. In this work, we tested the therapeutic role of Interleukin‐19 (IL‐19) in mice with MI and investigated the underlying molecular mechanism. Experimental approach Mice were subjected to MI by ligation of left anterior descending coronary artery (LAD) and treated with IL‐19 (10ng g‐1; i.p.). Key results Protein expression of IL‐19 and its receptor in myocardium were upregulated 24 hrs post‐MI in male mice. IL‐19 treatment decreased infarct and apoptosis in myocardium, accompanied by enhanced haem oxygenase‐1 (HO‐1) activities and reduced malondialdehyde (MDA) formation. Pretreatment with IL‐19 upregulated HO‐1 expression in cultured neonatal mouse ventricular myocytes and attenuated oxygen‐glucose deprivation (OGD)‐induced injuries in vitro. Furthermore, IL‐19 preserved cardiac function and improved survival of mice with MI. IL‐19 reduced inflammatory infiltrates and suppressed formation of TNF‐α, IL‐1β, and IL‐6. More importantly, IL‐19 inhibited polarization toward proinflammatory M1 macrophages and stimulated M2 macrophage polarization in myocardium of mice with MI. IL‐19 enhanced protein levels of vascular endothelial growth factor (VEGF) and promoted angiogenesis in myocardium of mice with MI. In addition, IL‐19 treatment increased DNA‐binding of the transcription factor STAT3 in myocardium of mice with MI. Conclusions and Implications Treatment with exogenous IL‐19 attenuated acute ischemic injury and improved survival of mice with MI. The mechanisms underlying these effects involved induction of HO‐1, M2 macrophage polarization, angiogenesis, and STAT3 activation.

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Interleukin-19 induces angiogenesis in the absence of hypoxia by direct and indirect immune mechanisms

Cited by 28 publications

References 46 publications

IL-20 receptor cytokines in autoimmune diseases

IL-20 receptor cytokines in autoimmune diseases

RNA stability protein ILF3 mediates cytokine‐induced angiogenesis

Exogenous IL‐19 attenuates acute ischaemic injury and improves survival in male mice with myocardial infarction

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