scholarly journals The expression of epithelial–mesenchymal transition–related proteins in biliary epithelial cells is associated with liver fibrosis in biliary atresia

2014 ◽  
Vol 77 (2) ◽  
pp. 310-315 ◽  
Author(s):  
Yongtao Xiao ◽  
Ying Zhou ◽  
Yingwei Chen ◽  
Kejun Zhou ◽  
Jie Wen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Epithelial Cells ◽  
Biliary Atresia ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells ◽  
Related Proteins

Epithelial-mesenchymal transition of biliary epithelial cells during cholestatic fibrosis

2007 ◽  
Vol 45 (01) ◽  
Author(s):  
F Schulze ◽  
E Konze ◽  
K Petmecky ◽  
K Schardt ◽  
O Dirsch ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

Toll-like receptor 4 shRNA attenuates lipopolysaccharide-induced epithelial-mesenchymal transition of intrahepatic biliary epithelial cells in rats

2018 ◽  
Vol 107 ◽  
pp. 1210-1217 ◽  
Author(s):  
Shifang Tang ◽  
Xiuhan Jiang ◽  
Lang Wu ◽  
Shifa Chen ◽  
Ling Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

scholarly journals Biliary Innate Immunity: Function and Modulation

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Kenichi Harada ◽  
Yasuni Nakanuma
Keyword(s):  
Innate Immunity ◽  
Epithelial Cells ◽  
Biliary Atresia ◽  
Th17 Cells ◽  
Bile Ducts ◽  
Innate Immune ◽  
Negative Regulator ◽  
Biliary Cirrhosis ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

Biliary innate immunity is involved in the pathogenesis of cholangiopathies in patients with primary biliary cirrhosis (PBC) and biliary atresia. Biliary epithelial cells possess an innate immune system consisting of the Toll-like receptor (TLR) family and recognize pathogen-associated molecular patterns (PAMPs). Tolerance to bacterial PAMPs such as lipopolysaccharides is also important to maintain homeostasis in the biliary tree, but tolerance to double-stranded RNA (dsRNA) is not found. In PBC, CD4-positive Th17 cells characterized by the secretion of IL-17 are implicated in the chronic inflammation of bile ducts and the presence of Th17 cells around bile ducts is causally associated with the biliary innate immune responses to PAMPs. Moreover, a negative regulator of intracellular TLR signaling, peroxisome proliferator-activated receptor-γ(PPARγ), is involved in the pathogenesis of cholangitis. Immunosuppression using PPARγligands may help to attenuate the bile duct damage in PBC patients. In biliary atresia characterized by a progressive, inflammatory, and sclerosing cholangiopathy, dsRNA viruses are speculated to be an etiological agent and to directly induce enhanced biliary apoptosis via the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Moreover, the epithelial-mesenchymal transition (EMT) of biliary epithelial cells is also evoked by the biliary innate immune response to dsRNA.

Epithelial-mesenchymal transition-related protein expression in biliary epithelial cells associated with hepatolithiasis

2014 ◽  
Vol 29 (2) ◽  
pp. 395-402 ◽  
Author(s):  
Rohyun Sung ◽  
Sang Hwa Lee ◽  
Meiying Ji ◽  
Joung-Ho Han ◽  
Min Ho Kang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protein Expression ◽  
Epithelial Mesenchymal Transition ◽  
Related Protein ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

LPS-Induced Epithelial-Mesenchymal Transition of Intrahepatic Biliary Epithelial Cells

2011 ◽  
Vol 171 (2) ◽  
pp. 819-825 ◽  
Author(s):  
Lijin Zhao ◽  
Rigao Yang ◽  
Long Cheng ◽  
Maijian Wang ◽  
Yan Jiang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

scholarly journals Interleukin-6 induces epithelial-mesenchymal transition in human intrahepatic biliary epithelial cells

2015 ◽  
Vol 13 (2) ◽  
pp. 1563-1569 ◽  
Author(s):  
GUI-XING JIANG ◽  
LI-PING CAO ◽  
PENG-CHENG KANG ◽  
XIANG-YU ZHONG ◽  
TIAN-YU LIN ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Interleukin 6 ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Biliary Epithelial Cells

scholarly journals Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Huijun Liu ◽  
Yuxiang Mao ◽  
Bing Xia ◽  
Chongde Long ◽  
Xielan Kuang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cellular Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Notch Pathway ◽  
Cyclin B1 ◽  
Lens Epithelial Cells ◽  
Smad Pathway ◽  
Mesenchymal Transition ◽  
Lens Extraction ◽  
Related Proteins

Background. Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO. Methods. Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR. Results. Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-β/Smad pathway and interfering Notch pathway which play important roles in PCO. Conclusions. This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO.

scholarly journals Fatty Acids and a High-Fat Diet Induce Epithelial–Mesenchymal Transition by Activating TGFβ and β-Catenin in Liver Cells

2021 ◽  
Vol 22 (3) ◽  
pp. 1272
Author(s):  
Oliwia Kwapisz ◽  
Judyta Górka ◽  
Agata Korlatowicz ◽  
Jerzy Kotlinowski ◽  
Agnieszka Waligórska ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Liver Fibrosis ◽  
Epithelial Cells ◽  
High Fat Diet ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Negative Regulator ◽  
Prolonged Treatment ◽  
High Fat ◽  
Mesenchymal Transition

Nonalcoholic fatty liver disease is defined as the accumulation of excessive fat in the liver in the absence of excessive alcohol consumption or any secondary cause. Although the disease generally remains asymptomatic, chronic liver inflammation leads to fibrosis, liver cirrhosis, and even to the development of hepatocellular carcinoma (HCC). Fibrosis results from epithelial–mesenchymal transition (EMT), which leads to dedifferentiation of epithelial cells into cells with a mesenchymal-like phenotype. During EMT, epithelial cells with high expression of E-cadherin, influenced by growth factors, cytokines, and inflammatory processes, undergo morphological changes via enhanced expression of, e.g., vimentin, fibronectin, and N-cadherin. An inducer of EMT and, consequently, of fibrosis development is transforming growth factor beta (TGFβ), a pleiotropic cytokine associated with the progression of hepatocarcinogenesis. However, the understanding of the molecular events that direct the development of steatosis into steatohepatitis and liver fibrosis remains incomplete. Our study revealed that both prolonged exposure of hepatocarcinoma cells to fatty acids in vitro and high-fat diet in mice (20 weeks) result in inflammation. Prolonged treatment with fatty acids increased the levels of TGFβ, MMP9, and β-catenin, important EMT inducers. Moreover, the livers of mice fed a high-fat diet exhibited features of liver fibrosis with increased TGFβ and IL-1 levels. Increased expression of IL-1 correlated with a decrease in monocyte chemoattractant protein-induced protein 1 (MCPIP1), a negative regulator of the inflammatory response that regulates the stability of proinflammatory transcripts encoding IL-1. Our study showed that a high-fat diet induced EMT by increasing the levels of EMT-activating transcription factors, including Zeb1, Zeb2, and Snail and changed the protein profile to a profile characteristic of the mesenchymal phenotype.

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