Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis

Qiulun Lu, Zejun Ma, Ye Ding, Tatiana Bedarida, Liming Chen, Zhonglin Xie (), Ping Song () and Ming-Hui Zou
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Qiulun Lu: Georgia State University
Zejun Ma: Georgia State University
Ye Ding: Georgia State University
Tatiana Bedarida: Georgia State University
Liming Chen: Tianjin Medical University
Zhonglin Xie: Georgia State University
Ping Song: Georgia State University
Ming-Hui Zou: Georgia State University

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract Although angiotensin II (AngII) is known to cause renal injury and fibrosis, the underlying mechanisms remain poorly characterized. Here we show that hypertensive nephropathy (HN) patients and AngII-infused mice exhibit elevated levels of circulating miR103a-3p. We observe a positive correlation between miR-103a-3p levels and AngII-induced renal dysfunction. miR-103a-3p suppresses expression of the sucrose non-fermentable-related serine/threonine-protein kinase SNRK in glomerular endothelial cells, and glomeruli of HN patients and AngII-infused mice show reduced endothelial expression of SNRK. We find that SNRK exerts anti-inflammatory effects by interacting with activated nuclear factor-κB (NF-κB)/p65. Overall, we demonstrate that AngII increases circulating miR-103a-3p levels, which reduces SNRK levels in glomerular endothelial cells, resulting in the over-activation of NF-κB/p65 and, consequently, renal inflammation and fibrosis. Together, our work identifies miR-103a-3p/SNRK/NF-κB/p65 as a regulatory axis of AngII-induced renal inflammation and fibrosis.

Date: 2019
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DOI: 10.1038/s41467-019-10116-0

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