Protein Inhibitor of Activated STAT3 Suppresses Oxidized LDL-induced Cell Responses during Atherosclerosis in Apolipoprotein E-deficient Mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11-15

AUTHORS

Rong Wang, Yanjin Zhang, Liran Xu, Yan Lin, Xiaofeng Yang, Liang Bai, Yulong Chen, Sihai Zhao, Jianglin Fan, Xianwu Cheng, Enqi Liu

ABSTRACT

Atherosclerosis is a serious public health concern. Excessive inflammatory responses of vascular cells are considered a pivotal pathogenesis mechanism underlying atherosclerosis development. It is known that Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signalling plays an important role in atherosclerosis progression. Protein inhibitor of activated STAT3 (PIAS3) is the key negative regulator of JAK/STAT3 signalling. However, its effect on atherogenesis is unknown. Here, we observed that PIAS3 levels are reduced in atherosclerotic lesions and that PIAS3 expression decreases in conjunction with increases in interleukin-6 expression and atherosclerosis severity. Oxidized low-density lipoprotein (ox-LDL), an atherogenic stimulus, reduced PIAS3 expression, an effect that may be attributed to nitric oxide synthesis upregulation. In turn, PIAS3 overexpression effectively suppressed ox-LDL-induced inflammation, lipid accumulation and vascular smooth muscle cell proliferation. These results indicate that PIAS3 is a critical repressor of atherosclerosis progression. The findings of this study have contributed to our understanding on the pathogenesis of atherosclerosis and have provided us with a potential target through which we can inhibit atherosclerosis-related cellular responses. More... »

PAGES

36790

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep36790

DOI

http://dx.doi.org/10.1038/srep36790

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1022401399

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27845432


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73 kinase/signal transducer
74 lesions
75 levels
76 lipid accumulation
77 lipoprotein
78 low-density lipoprotein
79 mechanism
80 mice
81 muscle cell proliferation
82 negative regulator
83 overexpression
84 pathogenesis
85 pathogenesis mechanisms
86 pathogenesis of atherosclerosis
87 potential target
88 progression
89 proliferation
90 protein inhibitor
91 public health concern
92 regulator
93 repressor
94 response
95 results
96 role
97 serious public health concern
98 severity
99 signal transducer
100 signaling
101 smooth muscle cell proliferation
102 stimuli
103 study
104 suppresses
105 target
106 transcription 3 (STAT3) signaling
107 transducer
108 turn
109 understanding
110 upregulation
111 vascular cells
112 vascular smooth muscle cell proliferation
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