miRNA-1246 suppresses acute lung injury-induced inflammation and apoptosis via the NF-κB and Wnt/β-catenin signal pathways

Suo, Tao; Chen, Guozhong; Huang, Yann-Chang; Zhao, Kaochang; Wang, Tao; Hu, Ke

doi:10.1016/j.biopha.2018.09.046

Cited by 52 publications

(37 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we known, Wnt/β-catenin activation mostly contributes to osteogenic differentiation and bone formation. 39,40 Furthermore, anti-inflammation function of Wnt/β-catenin by negative regulation of key master of inflammation-NFκB signalling was also found. 41,42 Studies demonstrated that overexpression of SFRP2 maintained the multi-lineage differentiation ability of MSCs and promoted engraftment, increased cardiac function in myocardial injury mice were also detected in vivo.…”

Section: Discussionmentioning

confidence: 90%

SFRP2 promotes stem cells from apical papilla‐mediated periodontal tissue regeneration in miniature pig

Han

Yang

et al. 2019

J of Oral Rehabilitation

View full text Add to dashboard Cite

Mesenchymal stem cell-based therapy is a reliable treatment for periodontal tissue regeneration, while ideal regeneration rate is still a facing problem. In previous study, we found SFRP2 a promising gene in modulating mesenchymal stem cells potential. We further investigated its role on periodontal tissue regeneration. We created periodontitis model in miniature pigs and locally injected with stem cells from apical papilla (SCAP). The periodontitis models were classed into three groups, SFRP2-SCAP group (injected with SCAP overexpressing with SFRP2), SCAP group (injected with SCAP transduced with vector backbone) and saline group (vehicle group injected with saline). Clinical assignment, CT scanning, histopathological assessment and quantitative analysis were applied to evaluate the regeneration effect. Twelve weeks after the injection, we found healthier gingival status in SFRP2-SCAP group than the other two groups. Clinical assignment results showed values of probing depth, gingival recession and attachment loss were improved in SFRP2-SCAP group than that of SCAP group and saline group. The volume of newborn bone was also enhanced in SFRP2-SCAP group than SCAP group and saline group. The difference of clinical assignments and newborn bone between each group was significant relevant. HE staining demonstrated increased tissue regeneration in SFRP2-SCAP group than SCAP group and saline group. Our findings revealed that SFRP2 could enhance SCAP-mediated periodontal tissue regeneration and provide a potential target for improving the regeneration of periodontal tissue.

show abstract

Section: Discussionmentioning

confidence: 90%

SFRP2 promotes stem cells from apical papilla‐mediated periodontal tissue regeneration in miniature pig

Han

Yang

et al. 2019

J of Oral Rehabilitation

View full text Add to dashboard Cite

show abstract

“…The mechanisms underlying abnormal inflammatory response are associated with activation of Toll-like receptor (TLR), mitogen-activated protein kinase (MAPK), protein kinase A, and nuclear factor (NF)-kB signal pathways. Lipopolysaccharide-induced acute lung injury is associated with suppression of Wnt/b-catenin pathway (Suo et al, 2018). Enhancing Wnt signaling is capable of attenuating TLR signaling and mediating the inflammatory response in lung alveolar epithelial cells (Li et al, 2014).…”

Section: Wnt Pathway In Copdmentioning

confidence: 99%

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

Gao

et al. 2019

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is a chronic lung disease with progressive airflow limitation and functional decline. The pathogenic mechanisms for this disease include oxidative stress, inflammatory responses, disturbed protease/antiprotease equilibrium, apoptosis/proliferation imbalance, senescence, autophagy, metabolic reprogramming, and mitochondrial dysfunction. The Wnt signaling pathway is an evolutionarily conserved signaling pathway that is abnormal in COPD, including chronic bronchitis and pulmonary emphysema. Furthermore, Wnt signaling has been shown to modulate aforementioned cellular processes involved in COPD. From this perspective, we provide an updated understanding of the crosstalk between Wnt signal and these cellular processes, and highlight the crucial role of the Wnt signal during the development of COPD. We also discuss the potential for targeting the Wnt signal in future translational and pharmacological therapeutics aimed at prevention and treatment of this disease.

show abstract

“…For example, miR-27a could alleviate lung inflammation and apoptosis in LPS-induced ALI mice by modulating the TLR4/MyD88/NF-κB pathway (28). Suo et al (29) have confirmed that miR-1246 could suppress ALI-induced inflammation and apoptosis by modulating NF-κB and Wnt/β-catenin pathways. In addition, miR-26a-5p is considered to be associated with inflammation and apoptosis in numerous diseases.…”

Section: Discussionmentioning

confidence: 99%

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

Yang

Fei

2020

Mol Med Rep

View full text Add to dashboard Cite

The aim of the present study was to investigate the regulatory functions of microRNA (miR)-26a-5p on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and its molecular mechanisms. The role of miR-26a-5p on an ALI mouse model was evaluated by examining the histological changes, wet/dry (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) expression levels in lung tissues and the survival of ALI mice. Moreover, the protein concentration and the number of neutrophils and lymphocytes in bronchoalveolar lavage fluid (BALF) was analyzed. To explore the effect of miR-26a-5p on inflammatory responses and apoptosis, the expression levels of tumour necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 and apoptosis were measured by ELISA, terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling staining and flow cytometry in BALF, A549 cells and lung tissues. B-cell lymphoma-2 (Bcl-2), Bax and cleaved caspase-3 in lung tissues were measured by western blotting and reverse transcription-quantitative PCR. Connective tissue growth factor (CTGF) was predicted as a direct target of miR-26a-5p using dual luciferase reporter assay. The present study sought to determine whether CTGF overexpression reversed the effect of miR-26a-5p on apoptosis and inflammatory responses in LPS-induced A549 cells. The data revealed that miR-26a-5p overexpression ameliorated LPS-induced ALI, which was implicated by fewer histopathological changes, W/D ratio, apoptosis in lung tissues and the survival of ALI mice. Moreover, miR-26a-5p overexpression alleviated LPS-induced inflammatory responses in ALI mice via the reduction of total protein, neutrophil and lymphocyte counts and the expression levels of TNF-α, IL-1β, IL-6, MDA and MPO activity in BALF. Similarly, miR-26a-5p overexpression decreased apoptosis and the expression of TNF-α, IL-1β and IL-6 in LPS-induced A549 cells. CTGF was a direct target of miR-26a-5p. CTGF overexpression reversed the effect of miR-26a-5p on cell apoptosis and inflammatory responses in LPS-induced A549 cells. The present study demonstrated that miR-26a-5p could attenuate lung inflammation and apoptosis in LPS-induced ALI by targeting CTGF.

show abstract

miRNA-1246 suppresses acute lung injury-induced inflammation and apoptosis via the NF-κB and Wnt/β-catenin signal pathways

Cited by 52 publications

References 27 publications

SFRP2 promotes stem cells from apical papilla‐mediated periodontal tissue regeneration in miniature pig

SFRP2 promotes stem cells from apical papilla‐mediated periodontal tissue regeneration in miniature pig

Perspectives on Wnt Signal Pathway in the Pathogenesis and Therapeutics of Chronic Obstructive Pulmonary Disease

miR‑26a‑5p alleviates lipopolysaccharide‑induced acute lung injury by targeting the connective tissue growth factor

Contact Info

Product

Resources

About