Alteration of Aging‐Dependent Micro<scp>RNA</scp>s in Idiopathic Pulmonary Fibrosis

Nho, Richard Seonghun

doi:10.1002/ddr.21272

Cited by 21 publications

(9 citation statements)

References 121 publications

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“…Instead, we found that level of circulating miR-29c-3p decrease in women (healthy controls) after age 50 compared to younger women. Taking into account the anti-fibrotic activity of miR-29, our data are consistent with the fact that fibrotic processes increase with advancing age (Nho, 2015). To evaluate the diagnostic effectiveness of potential markers, we performed a ROC analysis.…”

Section: Discussionsupporting

confidence: 80%

Peer Review #1 of "Combination of circulating miR-145-5p/miR-191-5p as biomarker for breast cancer detection (v0.2)"

Nassar¹

2020

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Section: Discussionsupporting

confidence: 80%

Peer Review #1 of "Combination of circulating miR-145-5p/miR-191-5p as biomarker for breast cancer detection (v0.2)"

Nassar¹

2020

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“…Notably, over 20 microRNAs including members of the miR-30, let-7, miR-29 families were decreased in IPF and lung cancer, commonly increased microRNAs included miR-155, miR-21, miR-205, and miR-31 ( 101 ). While the cellular origin and exact effects of all of these common microRNA changes are unclear, together with the observations about lung development, microRNA changes in the IPF lung suggest a loss of the differentiated organ regulatory networks potentially as a result of desynchronized aging ( 102 , 103 ).…”

Section: Role Of Non-coding Rnas In Ipfmentioning

confidence: 99%

Impact of Transcriptomics on Our Understanding of Pulmonary Fibrosis

Vukmirovic

Kaminski

2018

Front. Med.

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Idiopathic pulmonary fibrosis (IPF) is a lethal fibrotic lung disease characterized by aberrant remodeling of the lung parenchyma with extensive changes to the phenotypes of all lung resident cells. The introduction of transcriptomics, genome scale profiling of thousands of RNA transcripts, caused a significant inversion in IPF research. Instead of generating hypotheses based on animal models of disease, or biological plausibility, with limited validation in humans, investigators were able to generate hypotheses based on unbiased molecular analysis of human samples and then use animal models of disease to test their hypotheses. In this review, we describe the insights made from transcriptomic analysis of human IPF samples. We describe how transcriptomic studies led to identification of novel genes and pathways involved in the human IPF lung such as: matrix metalloproteinases, WNT pathway, epithelial genes, role of microRNAs among others, as well as conceptual insights such as the involvement of developmental pathways and deep shifts in epithelial and fibroblast phenotypes. The impact of lung and transcriptomic studies on disease classification, endotype discovery, and reproducible biomarkers is also described in detail. Despite these impressive achievements, the impact of transcriptomic studies has been limited because they analyzed bulk tissue and did not address the cellular and spatial heterogeneity of the IPF lung. We discuss new emerging technologies and applications, such as single-cell RNAseq and microenvironment analysis that may address cellular and spatial heterogeneity. We end by making the point that most current tissue collections and resources are not amenable to analysis using the novel technologies. To take advantage of the new opportunities, we need new efforts of sample collections, this time focused on access to all the microenvironments and cells in the IPF lung.

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“…Interestingly, these pathways have been shown to be controlled by miR-200 family members [21]. Y ang et al .…”

Section: Introductionmentioning

confidence: 99%

miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation

et al. 2019

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RationaleAlveolar type II (ATII) cells act as adult stem cells contributing to alveolar type I (ATI) cell renewal and play a major role in idiopathic pulmonary fibrosis (IPF), as supported by familial cases harbouring mutations in genes specifically expressed by these cells. During IPF, ATII cells lose their regenerative potential and aberrantly express pathways contributing to epithelial–mesenchymal transition (EMT). The microRNA miR-200 family is downregulated in IPF, but its effect on human IPF ATII cells remains unproven. We wanted to 1) evaluate the characteristics and transdifferentiating ability of IPF ATII cells, and 2) test whether miR-200 family members can rescue the regenerative potential of fibrotic ATII cells.MethodsATII cells were isolated from control or IPF lungs and cultured in conditions promoting their transdifferentiation into ATI cells. Cells were either phenotypically monitored over time or transfected with miR-200 family members to evaluate the microRNA effect on the expression of transdifferentiation, senescence and EMT markers.ResultsIPF ATII cells show a senescent phenotype (p16 and p21), overexpression of EMT (ZEB1/2) and impaired expression of ATI cell markers (AQP5 and HOPX) after 6 days of culture in differentiating medium. Transfection with certain miR-200 family members (particularly miR-200b-3p and miR-200c-3p) reduced senescence marker expression and restored the ability to transdifferentiate into ATI cells.ConclusionsWe demonstrated that ATII cells from IPF patients express senescence and EMT markers, and display a reduced ability to transdifferentiate into ATI cells. Transfection with certain miR-200 family members rescues this phenotype, reducing senescence and restoring transdifferentiation marker expression.

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Alteration of Aging‐Dependent MicroRNAs in Idiopathic Pulmonary Fibrosis

Cited by 21 publications

References 121 publications

Peer Review #1 of "Combination of circulating miR-145-5p/miR-191-5p as biomarker for breast cancer detection (v0.2)"

Peer Review #1 of "Combination of circulating miR-145-5p/miR-191-5p as biomarker for breast cancer detection (v0.2)"

Impact of Transcriptomics on Our Understanding of Pulmonary Fibrosis

miR-200 family members reduce senescence and restore idiopathic pulmonary fibrosis type II alveolar epithelial cell transdifferentiation

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