scholarly journals Epithelial-mesenchymal transition regulated by p38/MAPK signaling pathways participates in vasculogenic mimicry formation in SHG44 cells transfected with TGF-β cDNA loaded lentivirus in vitro and in vivo

2016 ◽  
Vol 49 (6) ◽  
pp. 2387-2398 ◽  
Author(s):  
Gengqiang Ling ◽  
Qiao Ji ◽  
Wei Ye ◽  
Dongying Ma ◽  
Yuena Wang
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Epithelial Mesenchymal Transition ◽  
Vasculogenic Mimicry ◽  
Mapk Signaling ◽  
Mesenchymal Transition ◽  
Mapk Signaling Pathways

scholarly journals Inhibition effects of patchouli alcohol against influenza a virus through targeting cellular PI3K/Akt and ERK/MAPK signaling pathways

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Yunjia Yu ◽  
Yang Zhang ◽  
Shuyao Wang ◽  
Wei Liu ◽  
Cui Hao ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Influenza A ◽  
Plaque Assay ◽  
Mapk Signaling ◽  
Western Blot Assay ◽  
Patchouli Alcohol ◽  
Erk Mapk ◽  
Mapk Signaling Pathways

Abstract Background Patchouli alcohol (PA) is a tricyclic sesquiterpene extracted from Pogostemonis Herba, which is a traditional Chinese medicine used for therapy of inflammatory diseases. Recent studies have shown that PA has various pharmacological activities, including anti-bacterial and anti-viral effects. Methods In this study, the anti-influenza virus (IAV) activities and mechanisms were investigated both in vitro and in vivo. The inhibitory effects of PA against IAV in vitro were evaluated by plaque assay and immunofluorescence assay. The neuraminidase inhibition assay, hemagglutination inhibition (HI) assay, and western blot assay were used to explore the anti-viral mechanisms. The anti-IAV activities in vivo were determined by mice pneumonia model and HE staining. Results The results showed that PA significantly inhibited different IAV strains multiplication in vitro, and may block IAV infection through inactivating virus particles directly and interfering with some early stages after virus adsorption. Cellular PI3K/Akt and ERK/MAPK signaling pathways may be involved in the anti-IAV actions of PA. Intranasal administration of PA markedly improved mice survival and attenuated pneumonia symptoms in IAV infected mice, comparable to the effects of Oseltamivir. Conclusions Therefore, Patchouli alcohol has the potential to be developed into a novel anti-IAV agent in the future.

scholarly journals Bone morphogenetic protein-7 prevented epithelial-mesenchymal transition in RLE-6TN cells

2016 ◽  
Vol 5 (3) ◽  
pp. 931-937 ◽  
Author(s):  
Yan Wang ◽  
Di Liang ◽  
Zhonghui Zhu ◽  
Xiaoli Li ◽  
Guoliang An ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Bone Morphogenetic Protein ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Epithelial Mesenchymal Transition ◽  
Bone Morphogenetic Protein 7 ◽  
Mesenchymal Transition ◽  
Morphogenetic Protein

Silica induced EMT and decreased the expression of BMP-7 in vivo and in vitro, while exogenous BMP-7 promoted MET and inhibited silica-induced EMT associated with inhibition of the p38 MAPK/transcription factor (TF) signaling pathway in RLE-6TN cells.

scholarly journals Hypoxia Activates Notch4 via ERK/JNK/P38 MAPK Signaling Pathways to Promote Lung Adenocarcinoma Progression and Metastasis

2021 ◽  
Vol 9 ◽  
Author(s):  
Xiaochen Li ◽  
Xiaopei Cao ◽  
Hanqiu Zhao ◽  
Mingzhou Guo ◽  
Xiaoyu Fang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Binding Interaction ◽  
Lung Cancer Patients ◽  
Cell Progression ◽  
Mapk Signaling Pathways

Hypoxia contributes to the progression and metastasis of lung adenocarcinoma (LUAD). However, the specific underlying molecular mechanisms have not been fully elucidated. Here we report that Notch4 is upregulated in lung tissue from lung cancer patients. Functionally, Hypoxia activates the expressions of Delta-like 4 and Notch4, resulting in the excessive proliferation and migration of LUAD cells as well as apoptotic resistance. Notch4 silencing reduced ERK, JNK, and P38 activation. Meanwhile, Notch4 overexpression enhanced ERK, JNK, and P38 activation in LUAD cells. Furthermore, Notch4 exerted pro-proliferation, anti-apoptosis and pro-migration effects on LUAD cells that were partly reversed by the inhibitors of ERK, JNK, and p38. The binding interaction between Notch4 and ERK/JNK/P38 were confirmed by the co-immunoprecipitation assay. In vivo study revealed that Notch4 played a key role in the growth and metastasis of LUAD using two xenograft models. This study demonstrates that hypoxia activates Notch4-ERK/JNK/P38 MAPK signaling pathways to promote LUAD cell progression and metastasis.

scholarly journals Berbamine Exerts Anti-Inflammatory Effects via Inhibition of NF-κB and MAPK Signaling Pathways

2017 ◽  
Vol 41 (6) ◽  
pp. 2307-2318 ◽  
Author(s):  
Xiao-Jian Jia ◽  
Xi Li ◽  
Feng Wang ◽  
Han-Qing Liu ◽  
Da-Jun Zhang
Keyword(s):  
Signaling Pathways ◽  
Mapk Signaling ◽  
Inflammatory Factor ◽  
Anti Inflammatory ◽  
Underlying Mechanisms ◽  
Peritonitis Model ◽  
Mapk Signaling Pathways ◽  
Superoxide Release

Background/Aims: This study aimed to investigate the anti-inflammatory activity of Berbamine (BER), a bisbenzylisoquinoline alkaloid extracted from Berberis amurensis (Xiao Bo An), and the underlying mechanisms. Methods: Macrophages and neutrophils were treated with BER in vitro and stimulated with LPS and fMLP. The effects of BER on the expression of pro-inflammatory mediators in macrophages were evaluated with quantitative RT-PCR and ELISA. The effects of BER on the activation and superoxide release of neutrophils were determined with flow cytometry and WST-1 reduction test. The inhibitory effects of BER on the activation of signaling pathways related to inflammatory response in macrophages were evaluated by western blot analysis. In addition, a mouse peritonitis model was made by peritoneal injection of thioglycollate medium and anti-inflammatory effects of BER were investigated in vivo by quantitative analysis of pro-inflammatory factor production and leukocyte exudation. Results: BER significantly inhibited inflammatory factor expression by LPS-stimulated macrophages and suppressed activation and superoxide release of fMLP-stimulated neutrophils. In the mouse peritonitis model, BER significantly inhibited the activation of macrophages and exudation of neutrophils. According to analysis, BER significantly suppressed phosphorylation of NF-κB and MAPK (JNK and ERK1/2) signaling pathways in LPS-stimulated macrophages. Conclusions: Collectively, data from this study suggest that BER has anti-inflammatory potential, which is effected via inhibition of NF-κB and MAPK signaling pathways, and thus holds promise for treatment of inflammatory disease.

scholarly journals CircEpc1 Promotes Ricin Toxin-Induced Inflammation via Activation of NF-κB and MAPK Signaling Pathways by Sponging miR-5114

2021 ◽  
Vol 12 ◽  
Author(s):  
Mingxin Dong ◽  
Xiaohao Zhang ◽  
Haotian Yu ◽  
Yan Wang ◽  
Ying Chang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Suppressive Effect ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Circular Rnas ◽  
Inflammatory Injury ◽  
Ricin Toxin ◽  
Mapk Signaling Pathways

Increasing studies have concentrated on investigating circular RNAs (circRNAs) as pivotal regulators in the progression of numerous diseases and biological processes and abundant evidence shows that circRNAs are participated in the regulation of innate immune responses. Several studies showed that Ricin Toxin (RT) could induce inflammatory injury. There was no research on the particular functions and underlying mechanisms of circRNAs in RT-induced inflammation. In this study, RNA sequencing performed on RT-treated and normal RAW264.7 macrophage cells was used to investigated the differentially expressed circRNAs. Based on the dataset, the expression of circEpc1 (mmu_circ_0,000,842) was identified higher in RT-treated cells. Moreover, gain-and-loss function assays showed that circEpc1 function as a promoter in RT-induced inflammation in vivo and in vitro. Mechanistically, circEpc1 acted as a miR-5114 sponge to relieve the suppressive effect of miR-5114 on its target NOD2 and thereby activating NF-κB and MAPK signaling pathways. Our results illuminated a link between RT-induced inflammation and the circEpc1 regulatory loop and provided novel insight into the functions of circRNA in innate immune, which may emerge as a potential target in immunotherapy to control the RT-induced inflammatory injury.

scholarly journals Tussilagone Inhibits Osteoclastogenesis and Periprosthetic Osteolysis by Suppressing the NF-κb and p38 MAPK Signaling Pathways

2019 ◽  
Author(s):  
Xuantao Hu ◽  
Zhengxiao Ouyang ◽  
Dan Peng ◽  
Ziqing Yin ◽  
Xia Chen ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Signaling Pathways ◽  
P38 Mapk ◽  
Western Blotting ◽  
Mapk Signaling ◽  
Luciferase Reporter ◽  
Periprosthetic Osteolysis ◽  
Prosthetic Loosening ◽  
Mapk Signaling Pathways

Abstract Backgroud: Aseptic prosthetic loosening is one of main factor producing poor prognosis of limb function after joint replacement and requiring troublesome revision surgery. It is featured by wear particle–induced periprosthetic osteolysis mediated by excessive osteoclasts activated in inflammatory cell context. In our previous study, some natural compounds showing anti-osteoclast trait with high cost-efficiency and few side effects. Tussilagone (TUS), as the main functional extract from Tussilago Farfara precedently used for relieving cough, asthma and eliminating phlegm in traditional medicine, has been proved to appease several RAW264.7-mediated inflammatory diseases via suppressing osteoclast-related signaling cascades. However, whether and how TUS can improve aseptic prosthetic loosening via modulating osteoclast-mediated bone resorption still need to be answered. Methods: We established a murine calvarial osteolysis model to detect the preventative effect of TUS on osteolysis in vivo. Micro-CT scanning and histomorphometric analysis were used to determine the variation of bone resorption and osteoclastogenesis in samples. The anti-osteoclast-differentiation and anti-bone-resorption bioactivities of TUS in vitro were investigated using bone slice resorption pit evaluation and interference caused by cytotoxicity of TUS was excluded according to CCK-8 assay. Quantitative PCR analysis was applied to prove the decreased expression of osteoclast-specific genes after TUS treatment. The inhibition effect of TUS on NF-κb and p38 MAPK signaling pathways was testified by western blotting and NF-κB-linked luciferase reporter gene assay.Results: TUS demonstrated bone protective effect against osteolysis in murine calvarial osteolysis model with reduced osteoclasts compared to the control group. Following studies in vitro witnessed that TUS exert anti-osteoclastogenesis and anti-bone-resorption effects in both BMMs and RAW264.7 cells, as evidenced by the decline of osteoclast specific genes according to quantative PCR. Western blotting revealed that TUS-treated demonstrated inhibited IκBα degradation and p38 phosphorylation.Conclusions: Collectively, for the first time our studies prove that TUS inhibits osteoclastogenesis by suppressing the NF-κb and p38 MAPK signaling pathways, therefore serving as a potential natural compound to treat periprosthetic osteolysis-induced aseptic prosthetic loosening.

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