The role of microRNAs in chronic respiratory disease: recent insights

Stolzenburg, Lindsay R.; Harris, Ann

doi:10.1515/hsz-2017-0249

Cited by 75 publications

(63 citation statements)

References 191 publications

(208 reference statements)

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“…10 In our study, the expression of miR-206 was upregulated in the lung tissues from COPD patients, which was a further confirmation on the previously study showing the upregulation of miR-206 in the plasma of COPD patients. 10 In our study, the expression of miR-206 was upregulated in the lung tissues from COPD patients, which was a further confirmation on the previously study showing the upregulation of miR-206 in the plasma of COPD patients.…”

Section: Discussionsupporting

confidence: 91%

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

Ying

et al. 2018

J of Cellular Biochemistry

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Chronic obstructive pulmonary disease (COPD) is a leading cause of death due to tis high morbidity and mortality. microRNAs have emerged as new biomarkers for the prognosis and diagnosis of patients with COPD. In this study, we aimed to investigate the expression of microRNA‐206 (miR‐206) in lung tissues from COPD patients and to explore the regulatory role of miR‐206 in the human pulmonary microvascular endothelial cells (HPMECs). Our results showed that cigarette smoke extract (CSE) promoted cell apoptosis, increased caspase‐3 activity, and upregulated the expression of miR‐206 in HPMECs, which was significantly reversed by the miR‐206 knockdown. Transfection with miR‐206 mimics led to cell apoptosis and was closely related to changes in the protein expression levels of caspase‐3, caspase‐9, and Bcl‐2 in HPMECs. Further bioinformatics prediction analysis revealed that the 3′‐untranslated region (3′UTR) of Notch3 and vascular endothelial growth factor‐A (VEGFA) harbored miR‐206‐binding sites, and overexpression of miR‐206 repressed the luciferase activity of the vectors containing Notch3 and VEGFA 3′UTR. Overexpression of either Notch3 or VEGFA attenuated miR‐206‐induced cell apoptosis in HPMECs. More importantly, miR‐206 expression was upregulated in the lung tissues from COPD patients and was positively corrected with forced expiratory volume 1% predicted in COPD patients, while Notch3 and VEGFA mRNA levels were downregulated and were negatively correlated with the expression level of miR‐206 in the lung tissues from COPD patients. In conclusion, our results showed that miR‐206 was upregulated in COPD patients and CSE‐treated HPMECs, promoted cell apoptosis via directly targeting Notch3 and VEGFA in HPMECs.

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Section: Discussionsupporting

confidence: 91%

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

Ying

et al. 2018

J of Cellular Biochemistry

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“…MicroRNAs (miRNAs) play important roles in regulating gene expression and specific miRNAs participate in the fibrotic process in different tissues and organs . MiRNA‐155 (miR‐155), a pro‐inflammatory factor via SHIP‐1 downregulation, has been identified as having immune regulatory functions and plays a critical role in tissue fibrosis in liver and lung .…”

Section: Introductionmentioning

confidence: 99%

“…MicroRNAs (miRNAs) play important roles in regulating gene expression and specific miRNAs participate in the fibrotic process in different tissues and organs. [7][8][9] MiRNA-155 (miR-155), a pro-inflammatory factor via SHIP-1 downregulation, has been identified as having immune regulatory functions and plays a critical role in tissue fibrosis in liver and lung. [10][11][12][13] However, contradictory effects of miR-155, pro-fibrotic and anti-fibrotic, in experimental and idiopathic pulmonary fibrosis, have been reported.…”

Section: Introductionmentioning

confidence: 99%

SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Tang

Mao

et al. 2019

FASEB j.

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Src Homology 2‐containing Inositol Phosphatase‐1 (SHIP‐1) is a target of miR‐155, a pro‐inflammatory factor. Deletion of the SHIP‐1 gene in mice caused spontaneous lung inflammation and fibrosis. However, the role and function of endothelial miR‐155 and SHIP‐1 in lung fibrosis remain unknown. Using whole‐body miR‐155 knockout mice and endothelial cell–specific conditional miR‐155 (VEC‐Cre‐miR‐155 or VEC‐miR‐155) or SHIP‐1 (VEC‐SHIP‐1) knockout mice, we assessed endothelial‐mesenchymal transition (EndoMT) and fibrotic responses in bleomycin (BLM) induced lung fibrosis models. Primary mouse lung endothelial cells (MLEC) and human umbilical vein endothelial cells (HUVEC) with SHIP‐1 knockdown were analyzed in TGF‐β1 or BLM, respectively, induced fibrotic responses. Fibrosis and EndoMT were significantly reduced in miR‐155KO mice and changes in EndoMT markers in MLEC after TGF‐β1 stimulation confirmed the in vivo findings. Furthermore, lung fibrosis and EndoMT responses were reduced in VEC‐miR‐155 mice but significantly enhanced in VEC‐SHIP‐1 mice after BLM challenge. SHIP‐1 knockdown in HUVEC cells resulted in enhanced EndoMT induced by BLM. Meanwhile, these changes involved the PI3K/AKT, JAK/STAT3, and SMAD/STAT signaling pathways. These studies demonstrate that endothelial miR‐155 plays an important role in fibrotic responses in the lung through EndoMT. Endothelial SHIP‐1 is essential in controlling fibrotic responses and SHIP‐1 is a target of miR‐155. Endothelial cells are an integral part in lung fibrosis.

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“…MicroRNAs have been recognized as important regulators in the gene regulation of COPD. 7 Downregulated miR128 in smokers, downregulated miR181d and miR30a-3p in COPD lung tissue, and increased miR223 in lungs of smokers have been demonstrated. 7 In a study investigating muscle wasting of COPD patients, the results showed that increased miR424-5p was associated with muscle wasting.…”

Section: Introductionmentioning

confidence: 97%

Systematic analysis of transcriptomic profiles of COPD airway epithelium using next-generation sequencing and bioinformatics

Chang¹,

Tsai²,

Jian³

et al. 2018

COPD

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IntroductionCOPD is a chronic inflammatory disease of lung. The inflammatory response in COPD is associated with neutrophils, macrophages, T lymphocytes, and bronchial epithelial cells, and occurs mainly in the small airway, leading to irreversible airflow limitation.MethodsIn order to investigate the microRNA–mRNA interaction in the microenvironment of the COPD airway, we used next-generation sequencing and bioinformatics in this study.ResultsWe identified four genes with microRNA–mRNA interactions involved in COPD small-airway bronchial epithelial cells: NT5E, SDK1, TNS1, and PCDH7. Furthermore, miR6511a-5p–NT5E interaction was found to be involved in small-airway bronchial epithelial cells, large-airway bronchial epithelial cells, and alveolar macrophages.ConclusionOur results showed that miR6511a-5p–NT5E interaction plays an important role in COPD, which might be associated with cell–cell contact, activation of leukocytes, activation of T lymphocytes, and cellular homeostasis. These findings provide new information for further investigations of the COPD microenvironment, and may help to develop new diagnostic or therapeutic strategies targeting the bronchial epithelium for COPD.

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The role of microRNAs in chronic respiratory disease: recent insights

Cited by 75 publications

References 191 publications

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

miRNA‐206 regulates human pulmonary microvascular endothelial cell apoptosis via targeting in chronic obstructive pulmonary disease

SHIP‐1, a target of miR‐155, regulates endothelial cell responses in lung fibrosis

Systematic analysis of transcriptomic profiles of COPD airway epithelium using next-generation sequencing and bioinformatics

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