MicroRNA-125b-5p modulates the inflammatory state of macrophages via targeting B7-H4

MicroRNA-125b-5p modulates the inflammatory state of macrophages via targeting B7-H4 As a newly identified negative costimulatory molecule of B7 family, B7-H4 suppresses T cell function via inhibiting cell proliferation and cytokine secretion. Although B7-H4 mRNA is widely distributed in various tissues, its protein expression is strongly limited, suggesting B7-H4 may be regulated post-transcriptionally. However, the mechanism underlying the inducement of B7-H4 expression remains unclear. In the present study, we identified specific targeting sites for miR-125b-5p in the 3′-UTR of B7-H4 gene, and showed that overexpression of miR-125b-5p downregulated B7-H4 expression in macrophages. We also demonstrated that in the activated macrophages, B7-H4 expression could be significantly induced by dexamethasone treatment post-transcriptionally, and that the induction of B7-H4 expression was accomplished by inversely correlated alteration of miR-125b-5p level. Additionally, our data showed that the inflammatory state of macrophages was enhanced by miR-125b-5p at least partially via targeting B7-H4. Taken together, our results demonstrated for the first time that miR-125b-5p could regulate the inflammatory state of macrophages via directly targeting B7-H4. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochemical and Biophysical Research Communications Elsevier

MicroRNA-125b-5p modulates the inflammatory state of macrophages via targeting B7-H4

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Publisher
Elsevier
Copyright
Copyright © 2017 Elsevier Inc.
ISSN
0006-291x
D.O.I.
10.1016/j.bbrc.2017.07.135
Publisher site
See Article on Publisher Site

Abstract

As a newly identified negative costimulatory molecule of B7 family, B7-H4 suppresses T cell function via inhibiting cell proliferation and cytokine secretion. Although B7-H4 mRNA is widely distributed in various tissues, its protein expression is strongly limited, suggesting B7-H4 may be regulated post-transcriptionally. However, the mechanism underlying the inducement of B7-H4 expression remains unclear. In the present study, we identified specific targeting sites for miR-125b-5p in the 3′-UTR of B7-H4 gene, and showed that overexpression of miR-125b-5p downregulated B7-H4 expression in macrophages. We also demonstrated that in the activated macrophages, B7-H4 expression could be significantly induced by dexamethasone treatment post-transcriptionally, and that the induction of B7-H4 expression was accomplished by inversely correlated alteration of miR-125b-5p level. Additionally, our data showed that the inflammatory state of macrophages was enhanced by miR-125b-5p at least partially via targeting B7-H4. Taken together, our results demonstrated for the first time that miR-125b-5p could regulate the inflammatory state of macrophages via directly targeting B7-H4.

Journal

Biochemical and Biophysical Research CommunicationsElsevier

Published: Sep 30, 2017

References

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