Comparison Analysis of Dysregulated LncRNA Profile in Mouse Plasma and Liver after Hepatic Ischemia/Reperfusion Injury

Chen, Zhenzhen; Luo, Yanjin; Yang, Weili; Ding, Linfang; Wang, Junpei; Tu, Jian; Geng, Bin; Cui, Qinghua; Yang, Jichun

doi:10.1371/journal.pone.0133462

Cited by 39 publications

(46 citation statements)

References 22 publications

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“…The precise regulatory mechanism remains unclear and further studies are needed to illuminate the exact mechanisms. Taken together, these results demonstrate that our In-cRNAs share similar features with those described in previous studies, in terms of structural, expression, and conservation properties (Alvarez-Dominguez et al, 2014;Yang et al, 2014;Chen et al, 2015).…”

Section: Discussionsupporting

confidence: 86%

The long non-coding RNA expression profile of Coxsackievirus A16 infected RD cells identified by RNA-seq

Shi

Xiong

et al. 2016

Virol. Sin.

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Coxsackievirus A16 (CVA16) is one of major pathogens of hand, foot and mouth disease (HFMD) in children. Long non-coding RNAs (IncRNAs) have been implicated in various biological processes, but they have not been associated with CVA16 infection. In this study, we comprehensively characterized the landscape of IncRNAs of normal and CVA16 infected rhabdomyosarcoma (RD) cells using RNA-Seq to investigate the functional relevance of IncRNAs. We showed that a total of 760 IncRNAs were upregulated and 1210 IncRNAs were downregulated. Out of these dysregulated IncRNAs, 43.64% were intergenic, 22.31% were sense, 15.89% were intronic, 8.67% were bidirectional, 5.59% were antisense, 3.85% were sRNA host IncRNAs and 0.05% were enhancer. Six dysregulated IncRNAs were validated by quantitative PCR assays and the secondary structures of these IncRNAs were projected. Moreover, we conducted a bioinformatics analysis of an IncRNAs (ENST00000602478) to elucidate the diversity of modification and functions of IncRNAs. In summary, the current study compared the dysregulated IncRNAs profile upon CVA16 challenge and illustrated the intricate relationship between coding and IncRNAs transcripts. These results may not only provide a complete picture of transcription in CVA16 infected cells but also provide novel molecular targets for treatments of HFMD.

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Section: Discussionsupporting

confidence: 86%

The long non-coding RNA expression profile of Coxsackievirus A16 infected RD cells identified by RNA-seq

Shi

Xiong

et al. 2016

Virol. Sin.

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“…Among transcripts, about 10-20% are the protein-coding RNAs, and the rest 80%-90% are non-protein-coding RNAs. Long non-coding RNA (lncRNA) is a kind of non encoding RNA longer than 200nt [3]. Recently, more and more evidences have showed that lncRNAs play a crucial part in tumorigenesis and progression of tumor.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma

et al. 2016

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Accumulating evidences indicate that long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) play important roles in tumorigenesis. However, the mechanisms remain largely unknown. To explore lncRNAs and circRNAs expression profiling and their biological functions in bladder cancer, we surveyed the lncRNA/circRNA and mRNA expression profiles of bladder cancer and para-cancer tissues using microarray for four patients. Thousands of significantly changed lncRNAs and mRNAs as well as hundreds of circRNAs were identified. Five dysregulated lncRNAs and four mRNAs were confirmed by quantitative real-time PCR in 30 pairs of samples. GO and KEGG pathway enrichment analyses were executed to determine the principal functions of the significantly deregulated genes. Further more, we constructed correlated expression networks including coding-noncoding co-expression (CNC), competing endogenous RNAs (ceRNA), cis regulation, lncRNAs-transcription factor (TF)-mRNA with bioinformatics methods. Co-expression analysis showed lncRNA APLP2 expression is correlated with apoptosis-related genes, including PTEN and TP53INP1. CeRNA network inferred that lncRNA H19 and circRNA MYLK could bind competitively with miRNA-29a-3p increasing target gene DNMT3B, VEGFA and ITGB1 expressions. Moreover, the nearby genes pattern displayed that overexpressing ADAM2 and C8orf4 are cis-regulated by lncRNA RP11-359E19.2, involving in progression of bladder cancer. In addition, lncRNAs-TF-mRNA diagram indicated that lncRNA BC041488 could trans-regulate CDK1 mRNA expression through SRF transcription factor. Taken together, these results suggested lncRNAs and circRNAs could implicate in the pathogenesis and development of bladder cancer. Our findings provide a novel perspective on lncRNAs and circRNAs and lay the foundation for future research of potential roles of lncRNAs and circRNAs in bladder carcinoma.

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“…Due to the fast development of basic medical research, the molecular mechanisms underlying the pathogenesis of testicular IRI have emerged gradually over the past few years. Extensive research has indicated that the dysregulation of lncRNAs may contribute to IRI progression in many systems [27-29]. Therefore, elucidating the role and biological functions of lncRNAs in testicular IRI is critical to better identify diagnostic tools and treatments in clinical settings.…”

Section: Discussionmentioning

confidence: 99%

MALAT1 Promotes Cell Apoptosis and Suppresses Cell Proliferation in Testicular Ischemia-Reperfusion Injury by Sponging MiR-214 to Modulate TRPV4 Expression

Ning

Fang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Accumulating evidences has indicated that aberrant expression of long non-coding RNAs (lncRNAs) is tightly associated with the progression of ischemia-reperfusion injury (IRI). Previous studies have reported that lncRNA MALAT1 regulates cell apoptosis and proliferation in myocardial and cerebral IRI. However, the underlying mechanism of MALAT1 in testicular IRI has not been elucidated. Methods: The levels of MALAT1, some related proteins and apoptosis in the testicular tissues were determined by quantitative real-time PCR, HE staining, immunohistochemistry, western blot and TUNEL assays. Relative expression of MALAT1, miR-214 and related proteins in cells were measured by western blot and quantitative real-time PCR. Cell viability and apoptosis were examined using MTT assay and flow cytometry. Results: In the present study, we found that MALAT1 was up-regulated in animal samples and GC-1 cells. The expression level of MALAT1 was positively related to cell apoptosis and negatively correlated with cell proliferation as testicular IRI progressed. In gain and loss of function assays, we confirmed that MALAT1 promotes cell apoptosis and suppresses cell proliferation in vitro and in vivo. Furthermore, we found that MALAT1 negatively regulates expression of miR-214 and promotes TRPV4 expression at the post-transcriptional level. Consequently, we investigated the correlation between MALAT1 and miR-214 and identified miR-214 as a direct target of MALAT1. In addition, we found that TRPV4 acted as a target of miR-214. Over-expression of miR-214 efficiently abrogated the up-regulation of TRPV4 induced by MALAT1, suggesting that MALAT1 positively regulates the expression of TRPV4 by sponging miR-214. Conclusion: In sum, our study indicated that the lncRNA MALAT1 promotes cell apoptosis and suppresses cell proliferation in testicular IRI via miR-214 and TRPV4.

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Comparison Analysis of Dysregulated LncRNA Profile in Mouse Plasma and Liver after Hepatic Ischemia/Reperfusion Injury

Cited by 39 publications

References 22 publications

The long non-coding RNA expression profile of Coxsackievirus A16 infected RD cells identified by RNA-seq

The long non-coding RNA expression profile of Coxsackievirus A16 infected RD cells identified by RNA-seq

Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma

MALAT1 Promotes Cell Apoptosis and Suppresses Cell Proliferation in Testicular Ischemia-Reperfusion Injury by Sponging MiR-214 to Modulate TRPV4 Expression

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