Upregulation of long noncoding RNA AP003419.16 predicts high risk of aging-associated idiopathic pulmonary fibrosis

Hao, Xiaoyan; Du, Ye; Li, Qian; Li, Dan; Liu, Xuejun

doi:10.3892/mmr.2017.7607

Cited by 21 publications

(18 citation statements)

References 38 publications

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“…Recently, lncRNA AP003419.16 was reported to be involved in the IPF process, but its underlying working mechanism still needs to be elucidated. 15 This study is a follow-up to previous research conducted in our laboratory. Our previous study was the first to report the different lncRNA profiles in IPF.…”

Section: Introductionmentioning

confidence: 90%

“…Interestingly, lncITPF expression increased with age, which could be due to the fact that age is the strongest demographic risk factor for IPF. Hao et al 15 also reported that lncRNA AP003419.16 regulates its adjacent gene RPS6KB2, which is involved in the process of aging and IPF. These findings are beneficial in determining whether the abnormal lncITPF can be taken as a biomarker or a therapeutic target for IPF.…”

Section: Several Lncrnas Have Been Discovered Through High-throughputmentioning

confidence: 99%

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lncITPF Promotes Pulmonary Fibrosis by Targeting hnRNP-L Depending on Its Host Gene ITGBL1

Song

Meng

et al. 2019

Molecular Therapy

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The role of long non-coding RNA (lncRNA) in idiopathic pulmonary fibrosis (IPF) is poorly understood. We found a novel lncRNA-ITPF that was upregulated in IPF. Bioinformatics and in vitro translation verified that lncITPF is an actual lncRNA, and its conservation is in evolution. Northern blot and rapid amplification of complementary DNA ends were used to analyze the full-length sequence of lncITPF. RNA fluorescence in situ hybridization and nucleocytoplasmic separation demonstrated that lncITPF was mainly located in the nucleus. RNA sequencing, chromatin immunoprecipitation (ChIP)-qPCR, CRISPR-Cas9 technology, and promoter activity analysis showed that the fibrotic function of lncITPF depends on its host gene integrin b-like 1 (ITGBL1), but they did not share the same promoter and were not co-transcribed. Luciferase activity, pathway inhibitors, and ChIP-qPCR showed that smad2/3 binds to the lncITPF promoter, and TGF-b1-smad2/3 was the upstream inducer of the fibrotic pathway. Furthermore, RNA-protein pull-down, liquid chromatography-mass spectrometry (LC-MS), and protein-RNA immunoprecipitation showed that lncITPF regulated H3 and H4 histone acetylation in the ITGBL1 promoter by targeting heterogeneous nuclear ribonucleoprotein L. Finally, sh-lncITPF was used to evaluate the therapeutic effect of lncITPF. Clinical analysis showed that lncITPF is associated with the clinicopathological features of IPF patients. Our findings provide a therapeutic target or diagnostic biomarker for IPF.

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Section: Introductionmentioning

confidence: 90%

Section: Several Lncrnas Have Been Discovered Through High-throughputmentioning

confidence: 99%

lncITPF Promotes Pulmonary Fibrosis by Targeting hnRNP-L Depending on Its Host Gene ITGBL1

Song

Meng

et al. 2019

Molecular Therapy

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“…Adhesion regulating molecule 1 (Adrm1) encodes the integral plasma membrane protein involved in proteolysis and deubiquitination [27–30]. It has been reported that Adrm1 is downregulated in ageing-associated idiopathic pulmonary fibrosis [31]. Furthermore, downregulation of Adrm1 at the mRNA and protein levels leads to slower wound-healing [32].…”

Section: Discussionmentioning

confidence: 99%

Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis

Xie

Zhao²,

Xie³

et al. 2019

Respir Res

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Background Lung injury due to zinc chloride smoke inhalation is very common in military personnel and leads to a high incidence of pulmonary complications and mortality. The aim of this study was to uncover the underlying mechanisms of lung injury due to zinc chloride smoke inhalation using a rat model. Methods: Histopathology analysis of rat lungs after zinc chloride smoke inhalation was performed by using haematoxylin and eosin (H&E) and Mallory staining. A lung injury rat model of zinc chloride smoke inhalation (smoke inhalation for 1, 2, 7 and 14 days) was developed. First, isobaric tags for relative and absolute quantization (iTRAQ) and weighted gene co-expression network analysis (WGCNA) were used to identify important differentially expressed proteins. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to study the biological functions of differentially expressed proteins. Then, analysis of lung injury repair-related differentially expressed proteins in the early (day 1 and day 2) and middle-late stages (day 7 and day 14) of lung injury after smoke inhalation was performed, followed by the protein-protein interaction (PPI) analysis of these differentially expressed proteins. Finally, the injury repair-related proteins PARK7 and FABP5 were validated by immunohistochemistry and western blot analysis. Results Morphological changes were observed in the lung tissues after zinc chloride smoke inhalation. A total of 27 common differentially expressed proteins were obtained on days 1, 2, 7 and 14 after smoke inhalation. WGCNA showed that the turquoise module (which involved 909 proteins) was most associated with smoke inhalation time. Myl3, Ckm, Adrm1 and Igfbp7 were identified in the early stages of lung injury repair. Gapdh, Acly, Tnni2, Acta1, Actn3, Pygm, Eno3 and Tpi1 (hub proteins in the PPI network) were identified in the middle-late stages of lung injury repair. Eno3 and Tpi1 were both involved in the glycolysis/gluconeogenesis signalling pathway. The expression of PARK7 and FABP5 was validated and was consistent with the proteomics analysis. Conclusion The identified hub proteins and their related signalling pathways may play crucial roles in lung injury repair due to zinc chloride smoke inhalation.

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“…The expression of lncRNA AP003419.16 and its adjacent gene RPS6KB2, increased significantly in patients with IPF. More importantly, AP003419.16 might increase the possibility of aging-associated IPF [13]. The lncRNA, CDKN2B-AS1, appears down-regulated in IPF patients compared with healthy controls.…”

Section: Lncrnas Can Regulate Target or Adjacent Gene In Ipfmentioning

confidence: 99%

Decrypting the crosstalk of noncoding RNAs in the progression of IPF

et al. 2020

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Idiopathic pulmonary fibrosis (IPF) is an agnogenic, rare, and lethal disease, with high mortality and poor prognosis and a median survival time as short as 3 to 5 years after diagnosis. No effective therapeutic drugs are still not available not only in clinical practice, but also in preclinical phases. To better and deeper understand pulmonary fibrosis will provide more effective strategies for therapy. Mounting evidence suggests that noncoding RNAs (ncRNAs) and their interactions may contribute to lung fibrosis; however, the mechanisms underlying their roles are largely unknown. In this review, we systematically summarized the recent advances regarding the crucial roles of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) and crosstalk among them in the development of IPF. The perspective for related genes was well highlighted. In summary, ncRNA and their interactions play a key regulatory part in the progression of IPF and are bound to provide us with new diagnostic and therapeutic targets.

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Upregulation of long noncoding RNA AP003419.16 predicts high risk of aging-associated idiopathic pulmonary fibrosis

Cited by 21 publications

References 38 publications

lncITPF Promotes Pulmonary Fibrosis by Targeting hnRNP-L Depending on Its Host Gene ITGBL1

lncITPF Promotes Pulmonary Fibrosis by Targeting hnRNP-L Depending on Its Host Gene ITGBL1

Identification of differentially expressed proteins in the injured lung from zinc chloride smoke inhalation based on proteomics analysis

Decrypting the crosstalk of noncoding RNAs in the progression of IPF

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