Sulforaphane inhibits cytokine-stimulated chemokine and adhesion molecule expressions in human corneal fibroblasts: Involvement of the MAPK, STAT, and NF-κB signaling pathways

2022 ◽  
pp. 108946
Author(s):  
Xiuxia Yang ◽  
Pingping Liu ◽  
Xiaojing Zhao ◽  
Chengcheng Yang ◽  
Binhui Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Corneal Fibroblasts

Baitouweng Decoction Alleviates Dextran Sulfate Sodium–Induced Ulcerative Colitis Through Nrf2/HO-1 Pathway Activation and HMGB1 Downregulation

2021 ◽  
Author(s):  
Weina Zhu ◽  
Chunhua Ma ◽  
Fuqiong Zhou ◽  
Jie Ruan ◽  
Yajie Zhang ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Aminosalicylic Acid

Abstract BackgroundThe phrase “baitouweng (BTW) decoction” was first recorded in the ancient Chinese medical text Shang Han Za Bing Lun. BTW decoction has been widely used by practitioners of (traditional) Chinese medicine.[VN1] It has been used to treat ulcerative colitis (UC) for hundreds of years. In this study, we investigated the antioxidative properties of BTW and the intestinal immunity of mice with dextran sulfate sodium (DSS)–induced UC and further investigated the mechanism by which BTW alleviates UC.MethodsUC was induced in mice by using DSS. The mice were randomly divided into the following five groups: control, DSS, BTW (5, 10, and 20 g/kg[VN2] ), berberine (BBR), and 5-aminosalicylic acid (5-ASA). Except for the control group, 3% DSS was administered in drinking water to all groups for 7 days, and and the other groups were intragastrically administered with BTW（5, 10, and 20 g/kg）、BBR and 5-ASA independently.[VN3] After gavaging for 12 days, the mice were killed. Subsequently, body weight loss, colon length, colon histopathology, inflammatory cytokine expression, and intestinal protein expression were measured.ResultsBTW effectively reduced the symptoms and histopathological scores of UC mice. Additionally, it downregulated the inflammatory factors interleukin (IL)-6 and IL-1β, the immunoglobulins vascular cell adhesion molecule 1 and intercellular adhesion molecule 1, and metalloprotease matrix metallopeptidase 9. Moreover, it downregulated high mobility group box 1 protein. Furthermore, it inhibited the nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.ConclusionBTW considerably alleviated the inflammatory symptoms of mice with acute colitis, and the latent mechanism of BTW may be related to various signaling pathways, including the modulation of antioxidant signaling pathways such as the Nrf2/HO-1 pathway.

Cytokine, Chemokine, and Adhesion Molecule Expression Mediated by MAPKs in Human Corneal Fibroblasts Exposed to Poly(I:C)

2008 ◽  
Vol 49 (8) ◽  
pp. 3336 ◽  
Author(s):  
Yang Liu ◽  
Kazuhiro Kimura ◽  
Ryoji Yanai ◽  
Tai-ichiro Chikama ◽  
Teruo Nishida
Keyword(s):  
Adhesion Molecule ◽  
Poly I:C ◽  
Adhesion Molecule Expression ◽  
Corneal Fibroblasts

Chemokine Signaling Pathways in Corneal Fibroblasts

2005 ◽  
Vol 3 (4) ◽  
pp. S-149-S-151 ◽  
Author(s):  
May Nour ◽  
James Chodosh
Keyword(s):  
Signaling Pathways ◽  
Chemokine Signaling ◽  
Corneal Fibroblasts

scholarly journals Neural Cell Adhesion Molecule Regulates Osteoblastic Differentiation Through Wnt/β-Catenin and PI3K-Akt Signaling Pathways in MC3T3-E1 Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Bin-Feng Cheng ◽  
Xiao Feng ◽  
Yao-Xin Gao ◽  
Shao-Qin Jian ◽  
Shi-Rao Liu ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Osteoblast Differentiation ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Osteoblastic Differentiation ◽  
Akt Signaling ◽  
Neural Cell ◽  
Neural Cell Adhesion

Neural cell adhesion molecule (NCAM) is involved in cell multi-directional differentiation, but its role in osteoblast differentiation is still poorly understood. In the present study, we investigated whether and how NCAM regulates osteoblastic differentiation. We found that NCAM silencing inhibited osteoblast differentiation in pre-osteoblastic MC3T3-E1 cells. The function of NCAM was further confirmed in NCAM-deficient mesenchymal stem cells (MSCs), which also had a phenotype with reduced osteoblastic potential. Moreover, NCAM silencing induced decrease of Wnt/β-catenin and Akt activation. The Wnt inhibitor blocked osteoblast differentiation, and the Wnt activator recovered osteoblast differentiation in NCAM-silenced MC3T3-E1 cells. We lastly demonstrated that osteoblast differentiation of MC3T3-E1 cells was inhibited by the PI3K-Akt inhibitor. In conclusion, these results demonstrate that NCAM silencing inhibited osteoblastic differentiation through inactivation of Wnt/β-catenin and PI3K-Akt signaling pathways.

Role of macrophage SR-BI class a scavenger receptor in atherosclerosis: Crosstalk TLR4/NF-KB/ signaling pathway activation   

2019 ◽  
Vol 7 (4) ◽  
pp. 298-309
Author(s):  
Jilin Wang ◽  
Jeffrey D. Juan
Keyword(s):  
Signaling Pathways ◽  
Adhesion Molecule ◽  
Intracellular Signaling ◽  
Scavenger Receptor ◽  
Cell Types ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Inflammatory Stimuli ◽  
Class B ◽  
Tlr4 Activation

Atherosclerosis is an inflammatory disease, and one of the culprits may be infections caused by pathogens, that may be linked to development and progression of atherosclerosis by several mechanisms. Class B scavenger receptor BI (SR-BI), an HDL receptor, SR-BI is expressed in a variety of cell types, most abundantly in steroidogenic cells and in the liver. SR-BI is also expressed in macrophages has been shown to mediate the cellular uptake of certain bacteria and may therefore play an important role in innate immunity. The innate immune response and the homeostatic network controlling cellular sterol are important implications for several common diseases, including atherosclerosis. The TLR4-independent SR-BI signaling in macrophages and the implication for its role in atherosclerosis has not yet to be investigated. Our data showed that mice lacking SR-BI are highly sensitive to form atherosclerosis than wild type mice. In addition, we showed that SR-BI-/- mice attenuated proinflammatory cytokines and chemokine response to LPS. The LPS-induced cytokine expression in both WT and SR-BI-/- was dependent on NFκB signaling pathways. One possibility is that an interaction between SR-BI and the TLR4 complex might modulate TLR4 activation and subsequent intracellular signaling pathways. The interaction of HDL and SR-BI in endothelial cells inhibits the activation of NFκB and subsequent expression of the adhesion molecules vascular cell adhesion molecule 1 and intercellular adhesion molecule 1 to inflammatory stimuli. We conclude that SR-BI plays an important function in the atherosclerosis mechanism.

Bile acids induce adhesion molecule expression in endothelial cells through activation of reactive oxygen species, NF-κB, and p38

2006 ◽  
Vol 291 (2) ◽  
pp. H741-H747 ◽  
Author(s):  
Pu Qin ◽  
Xiaoyan Tang ◽  
M. Merle Elloso ◽  
Douglas C. Harnish
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Bile Acid ◽  
Signaling Pathways ◽  
Bile Acids ◽  
Adhesion Molecule ◽  
Reactive Oxygen ◽  
Farnesoid X Receptor ◽  
Oxygen Species ◽  
Adhesion Molecule Expression

Bile acids are synthesized in the liver, stored in gallbladder, and secreted into the intestine to aid in the absorption of lipid-soluble nutrients. In addition, bile acids also actively participate in regulation of gene expression through their ability to act as ligands for the nuclear receptor farnesoid X receptor or by activating kinase signaling pathways. Under cholestatic conditions, elevated levels of bile acids in the liver induce hepatic inflammation, and because bile acid levels are also elevated in the circulation, they might also induce vascular inflammation. To test this hypothesis, primary human umbilical vein endothelial cells (HUVEC) and human aortic endothelial cells were treated with bile acids, and the expression of ICAM-1, VCAM-1, and E-selectin were monitored. The three major bile acids found in the circulation, chenodeoxycholic acid, deoxycholic acid, and lithocholic acid, all strongly induced both the mRNA and protein expression of ICAM-1 and VCAM-1. To delineate the mechanism, the experiments were conducted in the presence of various kinase inhibitors. The results demonstrate that the bile acid-mediated induction of adhesion molecule expression occurs by stimulation of NF-κB and p38 MAPK signaling pathways through the elevation in reactive oxygen species. The bile acid-induced cell surface expression of ICAM-1 and VCAM-1 was sufficient to result in the increased adhesion of THP-1 monocytes to the HUVEC, suggesting that elevated levels of bile acids in the circulation may cause endothelium dysfunction and contribute to the initiation of early events associated with vascular lesion formation.

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