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Endothelial dysfunction is critically involved in the pathogenesis of pulmonary arterial hypertension (PAH) and that exogenously administered microRNA may be of therapeutic benefit. Lower levels of miR‐483 were found in serum from patients with idiopathic pulmonary arterial hypertension (IPAH), particularly those with more severe disease. RNA‐seq and bioinformatics analyses showed that miR‐483 targets several PAH‐related genes, including transforming growth factor‐β (TGF‐β), TGF‐β receptor 2 (TGFBR2), β‐catenin, connective tissue growth factor (CTGF), interleukin‐1β (IL‐1β), and endothelin‐1 (ET‐1). Overexpression of miR‐483 in ECs inhibited inflammatory and fibrogenic responses, revealed by the decreased expression of TGF‐β, TGFBR2, β‐catenin, CTGF, IL‐1β, and ET‐1. In contrast, inhibition of miR‐483 increased these genes in ECs. Rats with EC‐specific miR‐483 overexpression exhibited ameliorated pulmonary hypertension (PH) and reduced right ventricular hypertrophy on challenge with monocrotaline (MCT) or Sugen + hypoxia. A reversal effect was observed in rats that received MCT with inhaled lentivirus overexpressing miR‐483. These results indicate that PAH is associated with a reduced level of miR‐483 and that miR‐483 might reduce experimental PH by inhibition of multiple adverse responses.
miR‐483, endothelium, pulmonary hypertension, TGF‐β
MicroRNA‐483 amelioration of experimental pulmonary hypertension
Jin Zhang, 1 , † Yangyang He, 2 , † Xiaosong Yan, 1 Shanshan Chen, 1 Ming He, 3 Yuyang Lei, 1 Jiao Zhang, 1 , 3 , 4 Brendan Gongol, 3 Mingxia Gu, 5 Yifei Miao, 5 Liang Bai, 1 Xiaopei Cui, 6 Xiaojian Wang, 2 Yixin Zhang, 2 Fenling Fan, 4 Zhao Li, 1 Yuan Shen, 7 Chih‐Hung Chou, 8 Hsien‐Da Huang, 9 Atul Malhotra, 3 Marlene Rabinovitch, 5 Zhi‐Cheng Jing,corresponding author 10 and John Y‐J Shyycorresponding author 1 , 3
2020 May 8;
Emerging evidence indicates that IGF2 plays an important role in various human malignancies, including colorectal cancer (CRC). Hsa-miR-483 is located within intron 7 of the IGF2 locus. However, the mechanism by which increased IGF2 induces carcinogenesis remains largely elusive. DLC-1 has been identified as a candidate tumor suppressor. In this study, we aimed at investigating whether miR-483 transcription is IGF2-dependent, identifying the functional target of miR-483, and evaluating whether tissue and serum miR-483-3p or miR-483-5p levels are associated with CRC. Our results showed that sequences upstream miR-483 had undetectable promoter activity and levels of IGF2, miR-483-3p, and miR-483-5p were synchronously increased in CRC tissues. Positive correlations between IGF2 and miR-483-3p (r=0.4984, ***p<0.0001), and between IGF2 and miR-483-5p (r=0.6659, ***p<0.0001) expression were found. In addition, patients with CRC had a significantly higher serum miR-483-5p level (*p<0.05) compared to normal controls. DLC-1 expression was decreased in colorectal cancer tissues and diminished through transient transfection with miR-483-3p. Our results suggest that IGF2 may exert its oncofunction, at least partly, through its parasitic miR-483 which suppressed DLC-1 in CRC cells. Thus, miR-483 might serve as a new target for therapy and a potential biomarker for the detection of colorectal cancer.
IGF2, miR-483, colorectal cancer, DLC-1
IGF2-derived miR-483 mediated oncofunction by suppressing DLC-1 and associated with colorectal cancer
Hengmi Cui,#1,2,7 Yuan Liu,#2,3,5 Jingrui Jiang,#2,3,6 Yangyang Liu,1,2 Zhe Yang,1,2 Shaogen Wu,2,3 Wangsen Cao,2 Isabelle H. Cui,4 and Chenggong Yu2,3
2016 Jul 26;
Calcific aortic valve disease (CAVD), characterized by aortic valve (AV) sclerosis and calcification, is a major cause of death in the aging population; however, there are no effective medical therapies other than valve replacement. AV calcification preferentially occurs on the fibrosa-side, exposed to disturbed flow (d-flow), while the ventricularis-side exposed to predominantly stable flow (s-flow) remains protected by unclear mechanisms. Here, we tested the role of novel flow-sensitive ubiquitin E2 ligase-C (UBE2C) and microRNA-483-3p (miR-483) in flow-dependent AV endothelial function and AV calcification.
Approach and Results:
Human AV endothelial cells (HAVECs) and fresh porcine AV (PAV) leaflets were exposed to s-flow or d-flow. We found that UBE2C was upregulated by d-flow in HAVECs in the miR-483-dependent manner. UBE2C mediated OS-induced endothelial inflammation and endothelial-mesenchymal-transition (EndMT) by increasing the hypoxia-inducible factor1α (HIF1α) level. UBE2C increased HIF1α by ubiquitinating and degrading its upstream regulator von Hippel-Lindau (pVHL). These in vitro findings were corroborated by immunostaining studies using diseased human AV leaflets. Additionally, we found that reduction of miR-483 by d-flow led to increased UBE2C expression in HAVECs. The miR-483 mimic protected against endothelial inflammation and EndMT in HAVECs and calcification of PAV leaflets by downregulating UBE2C. Moreover, treatment with the HIF1α inhibitor (PX478) significantly reduced PAV calcification in static and d-flow conditions.
These results suggest that miR-483 and UBE2C are novel flow-sensitive anti- and pro-CAVD molecules, respectively, that regulate the HIF1α pathway in AV. The miR-483 mimic and HIF1α pathway inhibitors may serve as potential therapeutics of CAVD.
Flow, AV endothelial cells, Ubiquitination, Inflammation, EndMT, AV calcification, miR-483, UBE2C, pVHL, HIF1α
Disturbed flow increases UBE2C via loss of miR-483-3p, inducing aortic valve calcification by the HIF1α pathway in endothelial cells
Joan Fernandez Esmerats,1 Nicolas Villa-Roel,1 Sandeep Kumar,1 Lina Gu,1 Md Tausif Salim,2 Michael Ohh,3 W. Robert Taylor,1,4 Robert M. Nerem,5 Ajit P. Yoganathan,1,2 and Hanjoong Jo1,4,†
2020 Mar 1.