miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells

Jiang, Jing; Song, Zhifang; Zhang, Lanyue

doi:10.12659/msm.910316

Cited by 13 publications

(12 citation statements)

References 32 publications

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“…MiR-155 plays crucial roles in the immune response, tumorigenesis and stem cell differentiation [33][34][35][36] and has been reported to target and repress many genes including SOCS1, TNF-α, and SHIP1 [18][19][20]. Dudda et al reported that miR-155 and its target gene, SOCS1, are key regulators of effector CD8( +) T cells as they affect cytokine signaling through STAT5 [37].…”

Section: Discussionmentioning

confidence: 99%

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Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Wang

Ling

Yao

et al. 2020

Virol J

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Background Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in infants, children, immunocompromised adults, and elderly individuals. Currently, there are few therapeutic options available to prevent RSV infection. The present study aimed to investigate the effects of luteolin on RSV replication and the related mechanisms. Material and methods We pretreated cells and mice with luteolin before infection with RSV, the virus titer, expressions of RSV-F, interferon (IFN)-stimulated genes (ISGs), and production of IFN-α and IFN-β were determined by plaque assay, RT-qPCR, and ELISA, respectively. The activation of Janus kinase (JAK)-signal transducer and activator of transcription 1 (STAT1) signaling pathway was detected by Western blotting and luciferase assay. Proteins which negatively regulate STAT1 were determined by Western blotting. Then cells were transfected with suppressor of cytokine signaling 1 (SOCS1) plasmid and virus replication and ISGs expression were determined. Luciferase reporter assay and Western blotting were performed to detect the relationship between SOCS1 and miR-155. Results Luteolin inhibited RSV replication, as shown by the decreased viral titer and RSV-F mRNA expression both in vitro and in vivo. The antiviral activity of luteolin was attributed to the enhanced phosphorylation of STAT1, resulting in the increased production of ISGs. Further study showed that SOCS1 was downregulated by luteolin and SOCS1 is a direct target of microRNA-155 (miR-155). Inhibition of miR-155 rescued luteolin-mediated SOCS1 downregulation, whereas upregulation of miR-155 enhanced the inhibitory effect of luteolin. Conclusion Luteolin inhibits RSV replication by regulating the miR-155/SOCS1/STAT1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

“…MiR-155 plays crucial roles in the immune response, tumorigenesis and stem cell differentiation [ 33 – 36 ] and has been reported to target and repress many genes including SOCS1, TNF-α, and SHIP1 [ 18 – 20 ]. Dudda et al .…”

Section: Discussionmentioning

confidence: 99%

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Wang

Ling

Yao

et al. 2020

Virol J

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“…Several immunomodulatory factors, released during ARDS, may reduce differentiation of MSCs into ATII-like cells and consequently attenuate therapeutic potential of MSCs in the treatment of ARDS. Overexpressed microRNA-615-3p or microRNA-155-5p inhibits differentiation of MSCs into ATII cells leading to the progression of ARDS [37, 38]. Pathological changes in the microenvironment of ARDS-injured lungs, in turn, negatively affect the capacity of MSCs to proliferate and differentiate into ATII cells [39].…”

Section: Msc-mediated Attenuation Of Ards and Pneumoniamentioning

confidence: 99%

Mesenchymal Stem Cell-Based Therapy of Inflammatory Lung Diseases: Current Understanding and Future Perspectives

Harrell

Sadikot

Pascual

et al. 2019

Stem Cells International

169

168

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During acute or chronic lung injury, inappropriate immune response and/or aberrant repair process causes irreversible damage in lung tissue and most usually results in the development of fibrosis followed by decline in lung function. Inhaled corticosteroids and other anti-inflammatory drugs are very effective in patients with inflammatory lung disorders, but their long-term use is associated with severe side effects. Accordingly, new therapeutic agents that will attenuate ongoing inflammation and, at the same time, promote regeneration of injured alveolar epithelial cells are urgently needed. Mesenchymal stem cells (MSCs) are able to modulate proliferation, activation, and effector function of all immune cells that play an important role in the pathogenesis of acute and chronic inflammatory lung diseases. In addition to the suppression of lung-infiltrated immune cells, MSCs have potential to differentiate into alveolar epithelial cells in vitro and, accordingly, represent new players in cell-based therapy of inflammatory lung disorders. In this review article, we described molecular mechanisms involved in MSC-based therapy of acute and chronic pulmonary diseases and emphasized current knowledge and future perspectives related to the therapeutic application of MSCs in patients suffering from acute respiratory distress syndrome, pneumonia, asthma, chronic obstructive pulmonary diseases, and idiopathic pulmonary fibrosis.

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“…MiRNAs are present in the circulatory system and changes in miRNA expression may herald the development of a variety of diseases including ALI (22,23). Cardinal-Fernández et al (24) have proposed that miRNAs are suitable biomarkers and therapeutic targets for ALI.…”

Section: Discussionmentioning

confidence: 99%

Improved Differentiation Ability and Therapeutic Effect of miR-23a-3p Expressing Bone Marrow-Derived Mesenchymal Stem Cells in Mice Model with Acute Lung Injury

Zhang

Liu

Yao

et al. 2021

IJSC

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Background and Objectives: Implantation of bone marrow-derived mesenchymal stem cells (BMSCs) has been recognized as an effective therapy for attenuating acute lung injury (ALI). This study aims to discover microRNA (miRNA)-mediated improvement of BMSCs-based therapeutic effects. Methods and Results: Mice were treated with lipopolysaccharide (LPS) for induction of ALI. BMSCs with lentivirus-mediated expression of miR-23b-3p or fibroblast growth factor 2 (FGF2) were intratracheally injected into the mice with ALI. The expressions of miR-23b-3p, FGF2, Occludin, and surfactant protein C (SPC) in lung tissues were analyzed by immunoblot or quantitative reverse transcription polymerase chain reaction. Histopathological changes in lung tissues were observed via hematoxylin-eosin staining. Lung edema was assessed by the ratio of lung wet weight/body weight (LWW/BW). The levels of interleukin (IL)-1β, IL-6, IL-4, and IL-8 in bronchoalveolar lavage fluid (BALF) were assessed by ELISA. LPS injection downregulated the expressions of miR-23b-3p, SPC and Occludin in the lung tissues, increased the LWW/BW ratio and aggravated histopathological abnormalities, while upregulating IL-1β, IL-6, IL-4, and IL-8 in the BALF. Upregulated miR-23b-3p counteracted LPS-induced effects, whereas downregulated miR-23b-3p intensified LPS-induced effects. FGF2, which was downregulated by miR-23b-3p upregulation, was a target gene of miR-23b-3p. Overexpressing FGF2 downregulated the expressions of miR-23b-3p, SPC and Occludin, increased the LWW/BW ratio and aggravated histopathological abnormalities, while upregulating IL-1β, IL-6, IL-4, and IL-8, and it offset miR-23b-3p upregulation-caused effects on the ALI mice. Conclusions: Overexpression of miR-23b-3p in BMSCs strengthened BMSC-mediated protection against LPS-induced mouse acute lung injury via targeting FGF2.

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miR-155-5p Promotes Progression of Acute Respiratory Distress Syndrome by Inhibiting Differentiation of Bone Marrow Mesenchymal Stem Cells to Alveolar Type II Epithelial Cells

Cited by 13 publications

References 32 publications

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Mesenchymal Stem Cell-Based Therapy of Inflammatory Lung Diseases: Current Understanding and Future Perspectives

Improved Differentiation Ability and Therapeutic Effect of miR-23a-3p Expressing Bone Marrow-Derived Mesenchymal Stem Cells in Mice Model with Acute Lung Injury

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