Interleukin-35 attenuates collagen-induced arthritis through suppression of vascular endothelial growth factor and its receptors
Copyright © 2016 Elsevier B.V. All rights reserved..
OBJECTIVE: To investigate the effect of interleukin-35 (IL-35) on vascular endothelial growth factor (VEGF) and its receptors, Flt-1 and Flk-1, in a collagen-induced arthritis (CIA) mouse model of rheumatoid arthritis (RA).
METHODS: We established a CIA mouse model and injected IL-35 intraperitoneally. The articular index (AI) was measured based on the amount of erythema, swelling, or joint rigidity and synovial histology was measured by hematoxylin and eosin staining (HE staining). The levels of VEGF, Flt-1, Flk-1, and von Willebrand factor (vWF) expression in CIA synovial tissue were determined by immunohistochemistry. The mRNA and protein expression levels of VEGF, Flt-1, Flk-1, TNF-α, and INF-γ were detected by reverse transcription PCR (RT-PCR) and western blots, respectively.
RESULTS: The IL-35 treatment decreased the AI and the synovial histological scores of CIA mice. Immunohistochemistry results revealed that the IL-35 treatment downregulated VEGF, Flt-1, Flk-1, and vWF expression in the CIA mice. RT-PCR results showed that the IL-35-treated mice had lower levels of VEGF, Flt-1, Flk-1, and TNF-α mRNA expression than those of the PBS-treated mice. While there was no significant difference in the level of INF-γ mRNA expression between IL-35-treated and PBS-treated mice. Western blot results showed that the IL-35 treatment downregulated the levels of VEGF, Flt-1, Flk-1, and TNF-α in CIA mice, but the level of INF-γ was not significantly affected.
CONCLUSION: These findings show that IL-35 may represent a novel therapeutic agent for RA, and the probable mechanisms may rely on inhibiting VEGF and its receptors Flt-1 and Flk-1.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2016 |
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| Erschienen: |
2016 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:34 |
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| Enthalten in: |
International immunopharmacology - 34(2016) vom: 27. Mai, Seite 71-77 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wu, Suqin [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 30.12.2016 Date Revised 12.05.2018 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.intimp.2016.02.018 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM257912533 |
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| 100 | 1 | |a Wu, Suqin |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Interleukin-35 attenuates collagen-induced arthritis through suppression of vascular endothelial growth factor and its receptors |
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| 500 | |a Date Completed 30.12.2016 | ||
| 500 | |a Date Revised 12.05.2018 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2016 Elsevier B.V. All rights reserved. | ||
| 520 | |a OBJECTIVE: To investigate the effect of interleukin-35 (IL-35) on vascular endothelial growth factor (VEGF) and its receptors, Flt-1 and Flk-1, in a collagen-induced arthritis (CIA) mouse model of rheumatoid arthritis (RA) | ||
| 520 | |a METHODS: We established a CIA mouse model and injected IL-35 intraperitoneally. The articular index (AI) was measured based on the amount of erythema, swelling, or joint rigidity and synovial histology was measured by hematoxylin and eosin staining (HE staining). The levels of VEGF, Flt-1, Flk-1, and von Willebrand factor (vWF) expression in CIA synovial tissue were determined by immunohistochemistry. The mRNA and protein expression levels of VEGF, Flt-1, Flk-1, TNF-α, and INF-γ were detected by reverse transcription PCR (RT-PCR) and western blots, respectively | ||
| 520 | |a RESULTS: The IL-35 treatment decreased the AI and the synovial histological scores of CIA mice. Immunohistochemistry results revealed that the IL-35 treatment downregulated VEGF, Flt-1, Flk-1, and vWF expression in the CIA mice. RT-PCR results showed that the IL-35-treated mice had lower levels of VEGF, Flt-1, Flk-1, and TNF-α mRNA expression than those of the PBS-treated mice. While there was no significant difference in the level of INF-γ mRNA expression between IL-35-treated and PBS-treated mice. Western blot results showed that the IL-35 treatment downregulated the levels of VEGF, Flt-1, Flk-1, and TNF-α in CIA mice, but the level of INF-γ was not significantly affected | ||
| 520 | |a CONCLUSION: These findings show that IL-35 may represent a novel therapeutic agent for RA, and the probable mechanisms may rely on inhibiting VEGF and its receptors Flt-1 and Flk-1 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Collagen-induced arthritis | |
| 650 | 4 | |a Interleukin-35 | |
| 650 | 4 | |a Rheumatoid arthritis | |
| 650 | 4 | |a Vascular endothelial growth factor | |
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| 650 | 7 | |a Von Willebrand antigen |2 NLM | |
| 650 | 7 | |a interleukin-35, mouse |2 NLM | |
| 650 | 7 | |a vascular endothelial growth factor A, mouse |2 NLM | |
| 650 | 7 | |a von Willebrand Factor |2 NLM | |
| 650 | 7 | |a Flt1 protein, mouse |2 NLM | |
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| 700 | 1 | |a Li, Yunxia |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Yuxuan |e verfasserin |4 aut | |
| 700 | 1 | |a Yao, Lutian |e verfasserin |4 aut | |
| 700 | 1 | |a Lin, Tiantian |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Shenyi |e verfasserin |4 aut | |
| 700 | 1 | |a Shen, Hui |e verfasserin |4 aut | |
| 700 | 1 | |a Xia, Liping |e verfasserin |4 aut | |
| 700 | 1 | |a Lu, Jing |e verfasserin |4 aut | |
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