Downregulating long non-coding RNA PVT1 expression inhibited the viability, migration and phenotypic switch of PDGF-BB-t
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RESEARCH ARTICLE
Downregulating long non‑coding RNA PVT1 expression inhibited the viability, migration and phenotypic switch of PDGF‑BB‑treated human aortic smooth muscle cells via targeting miR‑27b‑3p Shouming Li1 · Xin Zhao1 · Shaopeng Cheng1 · Jialiang Li1 · Xiao Bai1 · Xiangbin Meng1 Received: 28 May 2020 / Accepted: 14 October 2020 © Japan Human Cell Society 2020
Abstract Long non-coding RNA Plasmacytoma Variant Translocation 1 (LncRNA PVT1) was involved in various human diseases, but its role in aortic dissection (AD) remained to be fully examined. In this study, the viability and migration of human aortic smooth muscle cells (HASMCs) were respectively measured by MTT assay and wound-healing assay. Relative phenotypic switch-related protein expressions were measured with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. An AD model was established in animals and hematoxylin–eosin (H&E) staining was used for pathological examination. We found that, in HASMCs, microRNA (miR)-27b-3p could competitively bind with PVT1. In AD, PVT1 expression was upregulated, yet that of miR-27b-3p was downregulated. Downregulating PVT1 reversed the effects of growth factor-BB (PDGF-BB) treatment on PVT1, miR-27b-3p and expressions of phenotypic switch-related markers, and cell viability and migration, while downregulating miR-27b-3p reversed the effects of downregulating PVT1. Moreover, downregulating PVT1 suppressed the effects of upregulated PVT1 and downregulated miR-27b-3p induced by AD as well as media degeneration in vivo. In conclusion, downregulating PVT1 expression suppressed the proliferation, migration and phenotypic switch of HASMCs treated by PDGF-BB via targeting miR-27b-3p. Keywords Plasmacytoma Variant Translocation 1 · Platelet-derived growth factor-BB · Aortic dissection · Human aortic smooth muscle cells (HASMCs) · microRNA-27b-3p
Introduction As a critical aortic disease, aortic dissection (AD) involves the disruption on the medical layer of aortic wall and causes the intima separation from the adventitia, which tracks blood in a dissection plate within the media, thus causing aorta with true and false lumens [1]. AD will lead to a high mortality [2]. Currently, the development of drug adjunctive therapy has attracted much attention, as a lack of effective drug enables surgery, which is also accompanied with high
Shouming Li and Xin Zhao authors have contributed equally to this work. * Xin Zhao [email protected] 1
Department of Cardiovascular Surgery, Qilu Hospital of Shandong University, No.107, West Wenhua Road, Jinan 250012, Shandong, China
risk, to become the most commonly applied therapeutic treatment for AD [3]. Long non-coding RNAs (LncRNAs), with > 200 nucleotides in length, are a family of transcripts without proteincoding functions [4]. Many lncRNAs have been found to play a vital role in the pathogenesis of diseases related to aorta, including in AD [5]. As Zhang et al. pointed out, knocking down lncRNA taurine-up-regulated gene 1 (TUG1) could ameli
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