scholarly journals Chronic Arsenic Exposure and Angiogenesis in Human Bronchial Epithelial Cells via the ROS/miR-199a-5p/HIF-1 α /COX-2 Pathway

2014 ◽  
Vol 122 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Jun He ◽  
Min Wang ◽  
Yue Jiang ◽  
Qiudan Chen ◽  
Shaohua Xu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Arsenic Exposure ◽  
Bronchial Epithelial Cells ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Chronic Arsenic Exposure ◽  
Cox 2

scholarly journals Hepatocyte growth factor regulates cyclooxygenase-2 expression via β-catenin, Akt, and p42/p44 MAPK in human bronchial epithelial cells

2008 ◽  
Vol 294 (4) ◽  
pp. L778-L786 ◽  
Author(s):  
Young H. Lee ◽  
Yuichiro J. Suzuki ◽  
Autumn J. Griffin ◽  
Regina M. Day
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Gene Transcription ◽  
Bronchial Epithelial Cells ◽  
Cyclooxygenase 2 ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Cox 2 ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF) is upregulated in response to lung injury and has been implicated in tissue repair through its antiapoptotic and proliferative activities. Cyclooxygenase-2 (COX-2) is an inducible enzyme in the biosynthetic pathway of prostaglandins, and its activation has been shown to play a role in cell growth. Here, we report that HGF induces gene transcription of COX-2 in human bronchial epithelial cells (HBEpC). Treatment of HBEpC with HGF resulted in phosphorylation of the HGF receptor (c-Met), activation of Akt, and upregulation of COX-2 mRNA. Adenovirus-mediated gene transfer of a dominant negative (DN) Akt mutant revealed that HGF increased COX-2 mRNA in an Akt-dependent manner. COX-2 promoter analysis in luciferase reporter constructs showed that HGF regulation required the β-catenin-responsive T cell factor-4 binding element (TBE). The HGF activation of the COX-2 gene transcription was blocked by DN mutant of β-catenin or by inhibitors that blocked activation of Akt. Inhibition of p42/p44 MAPK pathway blocked HGF-mediated activation of β-catenin gene transcription but not Akt activation, suggesting that p42/p44 MAPK acts in a parallel mechanism for β-catenin activation. We also found that inhibition of COX-2 with NS-398 blocked HGF-induced growth in HBEpC. Together, the results show that the HGF increases COX-2 gene expression via an Akt-, MAPK-, and β-catenin-dependent pathway in HBEpC.

scholarly journals Aronia melanocarpa Fruit Bioactive Fraction Attenuates LPS-Induced Inflammatory Response in Human Bronchial Epithelial Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 816
Author(s):  
Bong-Keun Jang ◽  
Jin-Woo Lee ◽  
Hyun Choi ◽  
Sung-Vin Yim
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Aronia Melanocarpa ◽  
Tnf Α ◽  
Bioactive Fraction ◽  
Cox 2 ◽  
Oxide Synthase

To demonstrate the anti-inflammatory activity of Aronia melanocarpa fruit extract, human bronchial epithelial cells (BEAS-2B) were treated with lipopolysaccharide (LPS) and the effects of aronia bioactive fraction (ABF®), anthocyanin enriched extract from the fruit of A. melanocarpa, were evaluated. Following pretreatment with ABF® at 10–25 µg /mL, BEAS-2B cells were exposed to LPS and the expression of inflammatory mediators (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-8, regulated upon activation, normal T cell expressed and presumably secreted [RANTES], IL-1β, cyclooxygenase-2 [COX-2], and inducible nitric oxide synthase [iNOS]) was analyzed. In LPS-stimulated BEAS-2B cells, ABF® pretreatment significantly decreased the mRNA expression of TNF-α, IL-6, IL-8, RANTES, IL-1β, and COX-2 at doses of 10 and 25 µg/mL. ABF® also attenuated the secretion of TNF- α, IL-6, IL-8, and RANTES protein, as demonstrated by enzyme linked immunosorbent assay. Western blot analyses revealed the decreased expression of COX-2 and iNOS following ABF® treatment. ROS production was decreased, and the cell cycle was arrested at the G0/G1 and S phases following ABF® pretreatment. Our results suggest that ABF® may have potential as a nutraceutical agent for the suppression of airway inflammation.

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