Integrated analysis of non-coding RNAs for the identification of promising biomarkers in interstitial lung diseases

Mishra, Shailendra; Shah, Mohammad Imran; Sarkar, Malay; Rout, Chittaranjan

doi:10.1016/j.genrep.2018.03.002

Cited by 5 publications

(5 citation statements)

References 47 publications

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“…More and more evidence have suggested that lncRNAs could be novel biomarkers for diagnosis and treatment of various diseases [37][38][39][40]. Yu et al reported that lncRNA MALAT1 may increase cardiomyocyte autophagy and myocardial injury during I/R by negatively regulating miR-204 expression [20].…”

Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA TUG1 protects against cardiomyocyte ischaemia reperfusion injury by inhibiting HMGB1

Shi

Dong

Gao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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The aim of this study was to investigate whether lncRNA TUG1 could mediate the progression of ischemia-reperfusion injury following acute myocardial infraction. Mouse cardiomyocytes HL-1 cells were subjected to oxygen glucose deprivation followed by reperfusion (OGD/R) to induce myocardial I/R injury. The expression of TUG1 was detected by real-time PCR. Overexpression or down expression of TUG1 was performed in mouse HL-1 cardiomyocytes. The myocardial cell viability and apoptosis were respectively detected. In addition, the expression levels of inflammatory factors, apoptosis-related proteins and HMGB1 proteins were detected. Besides, an inhibitor of HMGB1 was used to treat cells to verify the relationship between TUG1 and HMGB1 protein. The expression of TUG1 was significantly up-regulated in OGD/R-induced myocardial HL-1 cells. The overexpression of TUG1-induced inflammation and apoptosis in OGD-R-induced myocardial HL-1 cells. Knock down of TUG1 protected OGD/Rinduced myocardial I/R injury by inhibiting HMGB1 expression. Suppression of lncRNA TUG1 may prevent myocardial I/R injury following acute myocardial infarction via inhibiting HMGB1 expression.

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Section: R E T R a C T E Dmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA TUG1 protects against cardiomyocyte ischaemia reperfusion injury by inhibiting HMGB1

Shi

Dong

Gao

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Characterization of potential biomarkers that have a strong correlation with DCGs was performed to validate and enhance the utility of this resource. Another case-study was also performed using a subset of ncRNAs and pathways from ILDgenDB ( 54 ). This study signified the role of ncRNAs (hsa-miR-1, hsa-miR-335-5p etc.)…”

Section: Resultsmentioning

confidence: 99%

“…Similarly, hsa-mir-575, hsa-mir-665, hsa-mir-4417 etc. found to be up-regulated in ILDs expression data when compared to healthy controls ( 54 ). These ncRNAs biomarkers may facilitate genetic-based disease monitoring and diagnosis.…”

Section: Resultsmentioning

confidence: 99%

ILDgenDB: integrated genetic knowledge resource for interstitial lung diseases (ILDs)

et al. 2018

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Interstitial lung diseases (ILDs) are a diverse group of ∼200 acute and chronic pulmonary disorders that are characterized by variable amounts of inflammation, fibrosis and architectural distortion with substantial morbidity and mortality. Inaccurate and delayed diagnoses increase the risk, especially in developing countries. Studies have indicated the significant roles of genetic elements in ILDs pathogenesis. Therefore, the first genetic knowledge resource, ILDgenDB, has been developed with an objective to provide ILDs genetic data and their integrated analyses for the better understanding of disease pathogenesis and identification of diagnostics-based biomarkers. This resource contains literature-curated disease candidate genes (DCGs) enriched with various regulatory elements that have been generated using an integrated bioinformatics workflow of databases searches, literature-mining and DCGs–microRNA (miRNAs)–single nucleotide polymorphisms (SNPs) association analyses. To provide statistical significance to disease-gene association, ILD-specificity index and hypergeomatric test scores were also incorporated. Association analyses of miRNAs, SNPs and pathways responsible for the pathogenesis of different sub-classes of ILDs were also incorporated. Manually verified 299 DCGs and their significant associations with 1932 SNPs, 2966 miRNAs and 9170 miR-polymorphisms were also provided. Furthermore, 216 literature-mined and proposed biomarkers were identified. The ILDgenDB resource provides user-friendly browsing and extensive query-based information retrieval systems. Additionally, this resource also facilitates graphical view of predicted DCGs–SNPs/miRNAs and literature associated DCGs–ILDs interactions for each ILD to facilitate efficient data interpretation. Outcomes of analyses suggested the significant involvement of immune system and defense mechanisms in ILDs pathogenesis. This resource may potentially facilitate genetic-based disease monitoring and diagnosis.Database URL: http://14.139.240.55/ildgendb/index.php

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“…Among the top 10 selected miRNAs, hsa-mir-155-5p, hsa-mir-16-5p and hsa-mir-26b-5p have been predicted to be involved in multiple pathways giving rise to interstitial lung diseases (ILD) and suggested as non-invasive biomarker (Mishra et al, 2018), hsa-mir-17-5p and hsa-mir-19a-3p have been shown to be involved in the prognosis of small cell lung cancer (Hayashita et al, 2005; Mancuso et al, 2016). Again, downregulation of hsa-mir-335-5p expression has been reported in COPD patients with PiZZ (Glu342Lys) inherited alpha1-antitrypsin deficiency (AATD) (Esquinas et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Integrated Bioinformatic Approach to Identify Potential Biomarkers against Idiopathic Pulmonary Fibrosis

Ullah

Sarkar

Araf

et al. 2019

Preprint

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Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive lung disease that leads to gradual decline in lung function. The molecular mechanism and risk factors of this disease are still obscure. Poorly understood etiology of this disease is the major obstacle in the identification of potential biomarkers and drug targets. In this study, microarray gene expression data of normal and IPF patient has been utilized for the statistical analysis of differentially expressed genes (DEGs) with a view to identifying potential molecular signatures using network-based system. Then their functional enrichment analysis revealed their predominant involvement in transcription, protein acetylation, extracellular matrix organization, apoptic process, inflammatory response etc. Protein-Protein Interaction (PPI) network revealed (UBC, PTEN, SOS1, PTK2, FGFR1, YAP1, FOXO1, RACK1, BMP4 and CD44) as hub proteins in IPF. Subsequent regulatory network analysis suggested (E2F1, STAT3, PPARG, MEF2A, FOXC1, GATA3, YY1, GATA2, NFKB1, and FOXL1) as the best regulatory transcriptional signatures and (hsa-mir-155-5p, hsa-mir-16-5p, hsa-mir-17-5p, hsa-mir-19a-3p, hsa-mir-192-5p, hsa-mir-92a-3p, hsa-mir-26b-5p, hsa-mir-335-5p, hsa-mir-124-3p, and hsa-let-7b-5p) as the best post-transcriptional signatures. This study represents proteome and RNA signatures of IPF which might be useful to uphold the present efforts in the discovery of potential biomarkers and treatments of this disease.

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Integrated analysis of non-coding RNAs for the identification of promising biomarkers in interstitial lung diseases

Cited by 5 publications

References 47 publications

RETRACTED ARTICLE: LncRNA TUG1 protects against cardiomyocyte ischaemia reperfusion injury by inhibiting HMGB1

RETRACTED ARTICLE: LncRNA TUG1 protects against cardiomyocyte ischaemia reperfusion injury by inhibiting HMGB1

ILDgenDB: integrated genetic knowledge resource for interstitial lung diseases (ILDs)

Integrated Bioinformatic Approach to Identify Potential Biomarkers against Idiopathic Pulmonary Fibrosis

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