scholarly journals Yi-Qi-Ping-Chuan-Fang Reduces TSLP Elevation Caused by LPS + Poly(I:C) via Inhibiting TLR4/MYD88/NF-κB Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Minye Qu ◽  
Xiang Tao ◽  
Jian Ma
Keyword(s):  
Signaling Pathways ◽  
Signaling Pathway ◽  
Primary Response ◽  
Poly I:C ◽  
Myeloid Differentiation ◽  
Bronchial Epithelial ◽  
Chinese Medicine Formula ◽  
Primary Response Gene ◽  
Protein Expressions ◽  
Related Proteins

Objective. To explore the correlation between Thymic Stromal Lymphopoietin (TSLP) and the Nuclear Factor- (NF-) κB signaling pathways in bronchial epithelial cells and to clarify whether the traditional Chinese medicine formula Yi-Qi-Ping-Chuan-Fang (YQPC) reduces inflammation by inhibiting TSLP/NF-κB signaling pathways. Methods. Cells were stimulated with LPS + Poly(I:C) and treated with YQPC. The expressions of TSLP and NF-κB signaling pathways related proteins P65, IκK, IκBa, P-P65, P-IκK, P-IκBa were detected. The effects of NF-κB upstream molecules, Toll-like receptors 3 and 4, myeloid differentiation primary response gene 88 (Myd88), TIR-domain-containing adapter-inducing interferon-β (TRIF), and downstream inflammatory cytokines, TNF-α, IL-1β, IL-6, and IL-8, were assessed. Results. The mRNA and protein expressions of TSLP were significantly increased after LPS + Poly(I:C) stimulation, the total protein IκBa and IκK decreased (P < 0.05), and the phosphorylated protein P-P65, P-IκK, and P-IκBα increased. After YQPC treatment, the expression of TSLP, P-P65, P-IκBa, and P-IκK was significantly inhibited (P < 0.05). The activation of TLR4 and MyD88 decreased, and release of IL-1β, IL-6, IL-8, and TNF-α reduced (P < 0.05). Conclusion. In summary, the expression of TSLP is activated by the NF-κB signaling pathway. YQPC alleviated inflammation by inhibiting TSLP through regulating the NF-κB activation and translocation.

Myeloid differentiation primary response gene 88 (MyD88) deficiency in a large kindred

2010 ◽  
Vol 126 (1) ◽  
pp. 172-175 ◽  
Author(s):  
Daniel H. Conway ◽  
Jasmeen Dara ◽  
Asen Bagashev ◽  
Kathleen E. Sullivan
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals Genetic Polymorphism in Extracellular Regulators of Wnt Signaling Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Garima Sharma ◽  
Ashish Ranjan Sharma ◽  
Eun-Min Seo ◽  
Ju-Suk Nam
Keyword(s):  
Genetic Polymorphism ◽  
Wnt Signaling ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
The Other ◽  
Present Review ◽  
Receptor Complex ◽  
Related Proteins ◽  
Related Association

The Wnt signaling pathway is mediated by a family of secreted glycoproteins through canonical and noncanonical mechanism. The signaling pathways are regulated by various modulators, which are classified into two classes on the basis of their interaction with either Wnt or its receptors. Secreted frizzled-related proteins (sFRPs) are the member of class that binds to Wnt protein and antagonizes Wnt signaling pathway. The other class consists of Dickkopf (DKK) proteins family that binds to Wnt receptor complex. The present review discusses the disease related association of various polymorphisms in Wnt signaling modulators. Furthermore, this review also highlights that some of the sFRPs and DKKs are unable to act as an antagonist for Wnt signaling pathway and thus their function needs to be explored more extensively.

MyD88, Myeloid Differentiation Primary Response Gene 88

2012 ◽  
pp. 1149-1159
Author(s):  
Andreas Gewies ◽  
Jürgen Ruland ◽  
Alexey Kotlyarov ◽  
Matthias Gaestel ◽  
Shiri Procaccia ◽  
...  
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals Sequence of MyD116 cDNA: a novel myeloid differentiation primary response gene induced by IL6

1990 ◽  
Vol 18 (9) ◽  
pp. 2823-2823 ◽  
Author(s):  
Kenneth A. Lord ◽  
Barbara Hoffman-Liebermann ◽  
Dan A. Liebermann
Keyword(s):  
Primary Response ◽  
Myeloid Differentiation ◽  
Response Gene ◽  
Primary Response Gene

Dispensable role of myeloid differentiation primary response gene 88 (MyD88) and MyD88-dependent toll-like receptors (TLRs) in a murine model of osteoarthritis

2014 ◽  
Vol 81 (4) ◽  
pp. 320-324 ◽  
Author(s):  
Sonia Nasi ◽  
Hang-Korng Ea ◽  
Véronique Chobaz ◽  
Peter van Lent ◽  
Frédéric Lioté ◽  
...  
Keyword(s):  
Murine Model ◽  
Primary Response ◽  
Myeloid Differentiation ◽  
Toll Like Receptors ◽  
Response Gene ◽  
Primary Response Gene

scholarly journals Alleviation by Mahuang Fuzi and Shenzhuo Decoction in High Glucose-Induced Podocyte Injury by Inhibiting the Activation of Wnt/β-Catenin Signaling Pathway, Resulting in Activation of Podocyte Autophagy

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Haoran Dai ◽  
Fei Liu ◽  
Xinping Qiu ◽  
Wenbin Liu ◽  
Zhaocheng Dong ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
High Glucose ◽  
Protective Mechanism ◽  
Podocyte Injury ◽  
Common Endpoint ◽  
Protein Expressions ◽  
Related Proteins ◽  
The Relationship ◽  
Excessive Activation ◽  
Organ Fibrosis

Background. Organ fibrosis is a common endpoint of a variety of diseases. Many studies have shown that the pathogenesis of diabetic kidney disease (DKD) is related to the excessive activation of the Wnt/β-catenin signaling pathway on podocytes, so the treatment of DKD starts from this signaling pathway. At the same time, DKD, as a metabolic disease, has many connections related to podocyte autophagy. Objectives. We experimented the effects of Mahuang Fuzi and Shenzhuo decoction (MFSD) which is the combination of Mahuang Fuzi decoction and Shenzhuo decoction in traditional Chinese medicine compounds used “The Golden Chamber” in high glucose-induced podocytes, determined whether this effect was related to Wnt/β-catenin signaling pathway, and further investigated the relationship between this effect and autophagy. Methods. The mice podocytes were stimulated by using 30 mmol/L of high glucose and serum containing MFSD or Wnt/β-catenin signaling pathway inhibitor DKK1 (100 ng/ml) was used to intervene podocytes before high glucose stimulation. Podocyte injury-related proteins, Wnt/β-catenin signaling pathway-related proteins, and autophagy-related proteins were detected by using western blotting and immunofluorescence analysis. Results. Our results showed that DKK1 and MFSD treatment significantly upregulated the protein expressions of nephrin, podocin, podocalyxin, and podoplanin in high glucose-induced podocytes and downregulated the β-catenin protein expression. Furthermore, the protein expressions of beclin1, LC3B, and P62 were also significantly increased in high glucose-induced podocytes. Conclusion. Our experiments confirmed that the destruction of podocytes in DKD is related to the excessive activation of Wnt/β-catenin signaling pathway and the inhibition of autophagy after activation. MFSD treatment can inhibit the activation of Wnt/β-catenin signaling pathway in podocytes stimulated by high glucose and helpful in reducing the podocyte injury. This protective mechanism can be related to the enhancement of podocyte autophagy by MFSD treatment.

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