Prospective vaccination of COVID-19 using shRNA-plasmid-LDH nanoconjugate

Aim: To explore whether shRNA targeting nonstructural protein (NSs) of severe fever with thrombocytopenia syndrome virus (SFTSV) could inhibit SFTSV replication in Vero cells. Materials & methods: SFTSV used in this experiment was propagated in Vero cells and stored at -20°C. shRNA plasmid against NSs of SFTSV was transfected to Vero cells and infected with SFTSV, after which western blotting and tissue culture infective dose (TCID50) were used to measure the virus titers. Results: shRNA against NSs protein decreased the expression of NSs and inhibited the replication of SFTSV. Conclusion: The constructed SFTSV NSs-shRNA plasmid could inhibit the replication of SFTSV. It was concluded that SFTSV NSs-shRNA could inhibit virus replication for at least 72 h. shRNA-mediated antiviral effects were dose-dependent.

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CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK, and AP-1 pathway

Arthritis Research & Therapy ◽

10.1186/s13075-020-02331-8 ◽

2020 ◽

Vol 22 (1) ◽

Author(s):

Sheng-Mou Hou ◽

Po-Chun Chen ◽

Chieh-Mo Lin ◽

Mei-Ling Fang ◽

Miao-Ching Chi ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Proinflammatory Cytokine ◽

Molecular Mechanisms ◽

Inflammatory Responses ◽

Synovial Fibroblasts ◽

Dependent Manner ◽

Tissue Samples ◽

Chemical Inhibitors ◽

Shrna Plasmid ◽

Signal Cascades

Abstract Background Osteoarthritis (OA) and rheumatoid arthritis (RA) are common joint disorders that are considered to be different diseases due to their unique molecular mechanisms and pathogenesis. Chemokines and their corresponding receptors have been well characterized in RA progression, but less so in OA pathogenesis. Methods The human primary synovial fibroblasts (SFs) were obtained from human OA and RA tissue samples. The Western blot and qPCR were performed to analyze the expression levels of CXCL1, as well as CXCL-promoted IL-6 expression in both OASFs and RASFs. The signal cascades that mediate the CXCL1-promoted IL-6 expression were identified by using chemical inhibitors, siRNAs, and shRNAs. Results Here, we found that both diseases feature elevated levels of CXCL1 and interleukin (IL)-6, an important proinflammatory cytokine that participates in OA and RA pathogenesis. In OASFs and RASFs, CXCL1 promoted IL-6 expression in a dose- and time-dependent manner. In OASFs and RASFs overexpressing CXCL1 or transduced with shRNA plasmid, IL-6 expression was markedly upregulated. CXCR2, c-Raf, and MAPKs were found to regulate CXCL1-induced IL-6 expression in OASFs and RASFs. Finally, CXCL1 triggered the transcriptional activities of c-Jun (which regulates the expression of proinflammatory proteins) in OASFs and RASFs. Conclusions Our present work suggests that the CXCL1/CXCR2 axis helps to orchestrate inflammatory responses in OA and RA SFs.

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Combination of LC3 shRNA Plasmid Transfection and Genistein Treatment Inhibited Autophagy and Increased Apoptosis in Malignant Neuroblastoma in Cell Culture and Animal Models

PLoS ONE ◽

10.1371/journal.pone.0078958 ◽

2013 ◽

Vol 8 (10) ◽

pp. e78958 ◽

Cited By ~ 22

Author(s):

Nishant Mohan ◽

Mrinmay Chakrabarti ◽

Naren L. Banik ◽

Swapan K. Ray

Keyword(s):

Cell Culture ◽

Animal Models ◽

Genistein Treatment ◽

Shrna Plasmid ◽

Plasmid Transfection

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CXCL1 contributes to IL-6 expression in osteoarthritis and rheumatoid arthritis synovial fibroblasts by CXCR2, c-Raf, MAPK and AP-1 pathway

10.21203/rs.3.rs-21874/v3 ◽

2020 ◽

Author(s):

Sheng-Mou Hou ◽

PoChun Chen ◽

Chieh-Mo Lin ◽

Mei-Ling Fang ◽

Miao-Ching Chi ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Proinflammatory Cytokine ◽

Molecular Mechanisms ◽

Inflammatory Responses ◽

Synovial Fibroblasts ◽

Dependent Manner ◽

Tissue Samples ◽

Chemical Inhibitors ◽

Shrna Plasmid ◽

Signal Cascades

Abstract Background: Osteoarthritis (OA) and rheumatoid arthritis (RA) are common joint disorders that are considered to be different diseases due to their unique molecular mechanisms and pathogenesis. Chemokines and their corresponding receptors have been well-characterized in RA progression, but less so in OA pathogenesis.Methods: The human primary synovial fibroblasts (SFs) were obtained from human OA and RA tissue samples. The Western blot and qPCR were performed to analyze expression levels of CXCL1, as well as CXCL-promoted IL-6 expression in both OASFs and RASFs. The signal cascades that mediate the CXCL1-promoted IL-6 expression were identified by using chemical inhibitors, siRNAs and shRNAs.Results: Here, we found that both diseases feature elevated levels of CXCL1 and interleukin (IL)-6, an important proinflammatory cytokine that participates in OA and RA pathogenesis. In OASFs and RASFs, CXCL1 promoted IL-6 expression in a dose- and time-dependent manner. In OASFs and RASFs overexpressing CXCL1 or transduced with shRNA plasmid, IL-6 expression was markedly upregulated. CXCR2, c-Raf and MAPKs was found to regulate CXCL1-induced IL-6 expression in OASFs and RASFs. Finally, CXCL1 triggered the transcriptional activities of c-Jun (which regulates the expression of proinflammatory proteins) in OASFs and RASFs.Conclusions: Our present work suggests that the CXCL1/CXCR2 axis helps to orchestrate inflammatory responses in OA and RA SFs.

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Transferrin-functionalized chitosan-graft-poly(l-lysine) dendrons as a high-efficiency gene delivery carrier for nasopharyngeal carcinoma therapy

Journal of Materials Chemistry B ◽

10.1039/c8tb00489g ◽

2018 ◽

Vol 6 (26) ◽

pp. 4314-4325 ◽

Cited By ~ 12

Author(s):

Tao Liu ◽

Shaohua Chen ◽

Siyi Zhang ◽

Xidong Wu ◽

Peina Wu ◽

...

Keyword(s):

Gene Therapy ◽

Nasopharyngeal Carcinoma ◽

Gene Delivery ◽

High Efficiency ◽

Shrna Plasmid

The co-polymer of transferrin-conjugated chitosan-graft-poly(l-lysine) dendrons was used to deliver the MMP-9 shRNA plasmid effectively for nasopharyngeal carcinoma gene therapy.

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Lipopolysaccharide-Binding Protein Downregulates Fractalkine through Activation of p38 MAPK and NF-κB

Mediators of Inflammation ◽

10.1155/2017/9734837 ◽

2017 ◽

Vol 2017 ◽

pp. 1-20 ◽

Cited By ~ 4

Author(s):

Xia Huang ◽

Yi Zeng ◽

Yujie Jiang ◽

Yueqiu Qin ◽

Weigui Luo ◽

...

Keyword(s):

P38 Mapk ◽

Lung Tissue ◽

Rat Model ◽

A549 Cells ◽

Rat Lung ◽

Rt Pcr ◽

Lipopolysaccharide Binding Protein ◽

Shrna Plasmid ◽

The Relationship ◽

Lps Treatment

Background. LBP and fractalkine are known to be involved in the pathogenesis of ARDS. This study investigated the relationship between LBP and fractalkine in LPS-induced A549 cells and rat lung tissue in an ARDS rat model. Methods. A549 cells were transfected with LBP or LBP shRNA plasmid DNA or pretreated with SB203580 or SC-514 following LPS treatment. An ARDS rat model was established using LPS with or without LBPK95A, SB203580, or SC-514 treatment. RT-PCR, western blotting, ELISA, immunofluorescence, coimmunoprecipitation, and immunohistochemical staining were used to study the expression of fractalkine and LBP and p38 MAPK and p65 NF-κB activities. Results. LPS increased LBP and reduced fractalkine. LBP overexpression further decreased LPS-induced downregulation of fractalkine and p38 MAPK and p65 NF-κB activation; LBP gene silencing, SB203580, and SC-514 suppressed LPS-induced downregulation of fractalkine and p38 MAPK and p65 NF-κB activation in A549 cells. LBP and fractalkine in lung tissue were increased and decreased, respectively, following LPS injection. LBPK95A, SB203580, and SC-514 ameliorated LPS-induced rat lung injury and suppressed LPS-induced downregulation of fractalkine by decreasing phospho-p38 MAPK and p65 NF-κB. Conclusions. The results indicate that LBP downregulates fractalkine expression in LPS-induced A549 cells and in an ARDS rat model through activation of p38 MAPK and NF-κB.

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