Profiling analysis of long non-coding RNAs in early postnatal mouse hearts

Sun, Xiongshan; Han, Qin; Luo, Hongqin; Pan, Xiaodong; Yan, Jing; Yao, Yang; Chen, Hanying; Wang, Fangjie; Lai, Wenjing; Guan, Xiao; Zhang, Qi; Tang, Yuan; Chu, Jian-Hong; Yu, Jianhua; Shou, Weinian; Deng, Youcai; Li, Xiaohui

doi:10.1038/srep43485

Cited by 12 publications

(12 citation statements)

References 55 publications

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“…Other noncoding RNAs such as lncRNAs (with more than 200 nucleotides in length) may also play a role in CM proliferation. LncRNA expressions significantly changed in cardiac hyperplastic to hypertrophic growth transition [ 35 ]. Manipulation of lncRNA-Gas5 and Sghrt in adult heart reduced the expression of cell cycle regulating genes including Ccng1 and Ccnd2 in CMs [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Noncoding RNA and Cardiomyocyte Proliferation

Zeng

Wang

2017

Stem Cells International

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It is acknowledged that postnatal mammalian cardiomyocytes (CMs) turn over with a very limited efficacy in both physiological and pathological conditions. Recent studies showed that those newly formed CMs are derived from preexisting CMs. Thus, stimulating CM proliferation becomes a promising strategy for inducing cardiac regeneration. Noncoding RNAs were found differently expressed in CMs with different proliferation potential. Moreover, manipulation of noncoding RNAs, in particular microRNAs, was proved to promote or suppress CM proliferation, indicating that noncoding RNAs are involved in the underlying mechanism of CM proliferation. This review mainly summarizes the roles of noncoding RNAs, as a class of influential factors, in the regulation of CM proliferation.

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Section: Discussionmentioning

confidence: 99%

Noncoding RNA and Cardiomyocyte Proliferation

Zeng

Wang

2017

Stem Cells International

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“…Extraction of carotid arteries and VSMCs were lysed with RIPA buffer (Beyotime Institute of Biotechnology) and then subjected to immunoblot analysis as described in our previous study [27]. Antibodies against Wip1, phospho (p)-S6 Ribosomal Protein (S6) Ser235/236 , total S6, p-4E-binding protein 1(4EBP1) Thr37/46 , total 4EBP1, TSC1, p-AMPKα Thr172 , AMPKα, p-AKT Thr308 , total AKT and β-actin were purchased from Cell Signaling Technology.…”

Section: Methodsmentioning

confidence: 99%

Wild-type p53-induced phosphatase 1 promotes vascular smooth muscle cell proliferation and neointima hyperplasia after vascular injury via p-adenosine 5′-monophosphate-activated protein kinase/mammalian target of rapamycin complex 1 pathway

Sun¹,

Li²,

Gan³

et al. 2019

Journal of Hypertension

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Objectives:Vascular smooth muscle cell (VSMC) proliferation is a crucial cause of vascular neointima hyperplasia and restenosis, thus limiting the long-term efficacy of percutaneous vascular intervention. We explored the role of wild-type p53-induced phosphatase 1 (Wip1), a potent regulator of tumorigenesis and atherosclerosis, in VSMC proliferation and neointima hyperplasia.Methods and results:Animal model of vascular restenosis was established in wild type C57BL/6J and VSMC-specific Tuberous Sclerosis 1 (TSC1)-knockdown mice by wire injury. We observed increased protein levels of Wip1, phospho (p)-S6 Ribosomal Protein (S6)Ser235/236, p-4EBP1Thr37/46 but decreased p-adenosine 5′-monophosphate-activated protein kinase (AMPK)αThr172 both in carotid artery at day 28 after injury and in VSMCs after 48 h of platelet derived growth factor-BB (PDGF-BB) treatment. By using hematoxylin-eosin staining, Ki-67 immunohistochemical staining, cell counting kit-8 assay and Ki-67 immunofluorescence staining, we found Wip1 antagonist GSK2830371 (GSK) or mammalian target of rapamycin complex 1 (mTORC1) inhibitor rapamycin both obviously reversed the neointima formation and VSMC proliferation induced by wire injury and PDGF-BB, respectively. GSK also reversed the increase in mRNA level of Collagen I after wire injury. However, GSK had no obvious effects on VSMC migration induced by PDGF-BB. Simultaneously, TSC1 knockdown as well as AMPK inhibition by Compound C abolished the vascular protective and anti-proliferative effects of Wip1 inhibition. Additionally, suppression of AMPK also reversed the declined mTORC1 activity by GSK.Conclusion:Wip1 promotes VSMC proliferation and neointima hyperplasia after wire injury via affecting AMPK/mTORC1 pathway.

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“…To conduct enrichment analyses, the package cluster Profiler (version 3.2.14) of R (version 3.3.3) was used for analyzing the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and Gene Ontology (GO) processes, as described previously 24 , 25 .…”

Section: Methodsmentioning

confidence: 99%

Development Of A Three-Gene Prognostic Signature For Hepatitis B Virus Associated Hepatocellular Carcinoma Based On Integrated Transcriptomic Analysis

Yao¹,

Lü²,

Shao

et al. 2018

J. Cancer

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Integration of public genome-wide gene expression data together with Cox regression analysis is a powerful weapon to identify new prognostic gene signatures for cancer diagnosis and prognosis. Hepatitis B virus (HBV) is a major cause of hepatocellular carcinoma (HCC), however, it remains largely unknown about the specific gene prognostic signature of HBV-associated HCC. Using Robust Rank Aggreg (RRA) method to integrate seven whole genome expression datasets, we identified 82 up-regulated genes and 577 down-regulated genes in HBV-associated HCC patients. Combination of several enrichment analysis, univariate and multivariate Cox proportional hazards regression analysis, we revealed that a three-gene (SPP2, CDC37L1, and ECHDC2) prognostic signature could act as an independent prognostic indicator for HBV-associated HCC in both the discovery cohort and the internal testing cohort. Gene set enrichment analysis showed that the high-risk group with lower expression levels of the three genes was enriched in bladder cancer and cell cycle pathway, whereas the low-risk group with higher expression levels of the three genes was enriched in drug metabolism-cytochrome P450, PPAR signaling pathway, fatty acid and histidine metabolisms. This indicates that patients of HBV-associated HCC with higher expression of these three genes may preserve relatively good hepatic cellular metabolism and function, which may also protect HCC patients from persistent drug toxicity in response to various medication. Our findings suggest a three-gene prognostic model that serves as a specific prognostic signature for HBV-associated HCC.

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Profiling analysis of long non-coding RNAs in early postnatal mouse hearts

Cited by 12 publications

References 55 publications

Noncoding RNA and Cardiomyocyte Proliferation

Noncoding RNA and Cardiomyocyte Proliferation

Wild-type p53-induced phosphatase 1 promotes vascular smooth muscle cell proliferation and neointima hyperplasia after vascular injury via p-adenosine 5′-monophosphate-activated protein kinase/mammalian target of rapamycin complex 1 pathway

Development Of A Three-Gene Prognostic Signature For Hepatitis B Virus Associated Hepatocellular Carcinoma Based On Integrated Transcriptomic Analysis

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