miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis
Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also f...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2016-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2016/8060182 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1849410433545404416 |
|---|---|
| author | Jinshan Ye Ruiwei Guo Yankun Shi Feng Qi Chuanming Guo Lixia Yang |
| author_facet | Jinshan Ye Ruiwei Guo Yankun Shi Feng Qi Chuanming Guo Lixia Yang |
| author_sort | Jinshan Ye |
| collection | DOAJ |
| description | Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α. Downregulation of miR-155 and PDCD4 and upregulation of SOCS1 obviously decreased the IL-6 and TNF-α expression. In addition, inhibition of miR-155 levels in atherosclerotic mice could notably reduce the IL-6 and TNF-α level in plasma and aortic tissue, accompanied with increased p-STAT3 and PDCD4 and decreased SOCS1. Thus, miR-155 might mediate the inflammation in AS via the SOCS1-STAT3-PDCD4 axis. These results provide a rationale for intervention of intracellular miR-155 as possible antiatherosclerotic targets. |
| format | Article |
| id | doaj-art-80eba1b5aea8483790935f21a607387e |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-80eba1b5aea8483790935f21a607387e2025-08-20T03:35:07ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/80601828060182miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in AtherogenesisJinshan Ye0Ruiwei Guo1Yankun Shi2Feng Qi3Chuanming Guo4Lixia Yang5Department of Postgraduate, Third Military Medical University, Chongqing 400038, ChinaDepartment of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, ChinaDepartment of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, ChinaDepartment of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, ChinaDepartment of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, ChinaDepartment of Postgraduate, Third Military Medical University, Chongqing 400038, ChinaInflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-α. Downregulation of miR-155 and PDCD4 and upregulation of SOCS1 obviously decreased the IL-6 and TNF-α expression. In addition, inhibition of miR-155 levels in atherosclerotic mice could notably reduce the IL-6 and TNF-α level in plasma and aortic tissue, accompanied with increased p-STAT3 and PDCD4 and decreased SOCS1. Thus, miR-155 might mediate the inflammation in AS via the SOCS1-STAT3-PDCD4 axis. These results provide a rationale for intervention of intracellular miR-155 as possible antiatherosclerotic targets.http://dx.doi.org/10.1155/2016/8060182 |
| spellingShingle | Jinshan Ye Ruiwei Guo Yankun Shi Feng Qi Chuanming Guo Lixia Yang miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis Mediators of Inflammation |
| title | miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis |
| title_full | miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis |
| title_fullStr | miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis |
| title_full_unstemmed | miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis |
| title_short | miR-155 Regulated Inflammation Response by the SOCS1-STAT3-PDCD4 Axis in Atherogenesis |
| title_sort | mir 155 regulated inflammation response by the socs1 stat3 pdcd4 axis in atherogenesis |
| url | http://dx.doi.org/10.1155/2016/8060182 |
| work_keys_str_mv | AT jinshanye mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis AT ruiweiguo mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis AT yankunshi mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis AT fengqi mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis AT chuanmingguo mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis AT lixiayang mir155regulatedinflammationresponsebythesocs1stat3pdcd4axisinatherogenesis |