scholarly journals ATF3 represses PINK1 gene transcription in lung epithelial cells to control mitochondrial homeostasis

Aging Cell ◽  
2018 ◽  
Vol 17 (2) ◽  
pp. e12720 ◽  
Author(s):  
Marta Bueno ◽  
Judith Brands ◽  
Lauren Voltz ◽  
Kaitlin Fiedler ◽  
Brenton Mays ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Gene Transcription ◽  
Lung Epithelial Cells ◽  
Mitochondrial Homeostasis ◽  
Lung Epithelial ◽  
Pink1 Gene

Nitric oxide increases IL-8 gene transcription and mRNA stability to enhance IL-8 gene expression in lung epithelial cells

2004 ◽  
Vol 287 (4) ◽  
pp. L764-L773 ◽  
Author(s):  
Loretta Sparkman ◽  
Vijayakumar Boggaram
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Gene Transcription ◽  
Mrna Stability ◽  
Inflammatory Responses ◽  
Lung Epithelial Cells ◽  
Mrna Levels ◽  
Lung Epithelial

Interleukin (IL)-8, a C-X-C chemokine, is a potent chemoattractant and an activator for neutrophils, T cells, and other immune cells. The airway and respiratory epithelia play important roles in the initiation and modulation of inflammatory responses via production of cytokines and surfactant. The association between elevated levels of nitric oxide (NO) and IL-8 in acute lung injury associated with sepsis, acute respiratory distress syndrome, respiratory syncytial virus infection in infants, and other inflammatory diseases suggested that NO may play important roles in the control of IL-8 gene expression in the lung. We investigated the role of NO in the control of IL-8 gene expression in H441 lung epithelial cells. We found that a variety of NO donors significantly induced IL-8 mRNA levels, and the increase in IL-8 mRNA was associated with an increase in IL-8 protein. NO induction of IL-8 mRNA was due to increases in IL-8 gene transcription and mRNA stability. NO induction of IL-8 mRNA levels was not inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and KT-5823, inhibitors of soluble guanylate cyclase and protein kinase G, respectively, and 8-bromo-cGMP did not increase IL-8 mRNA levels. This indicated that NO induces IL-8 mRNA levels independently of changes in the intracellular cGMP levels. NO induction of IL-8 mRNA was significantly reduced by inhibitors of extracellular regulated kinase and protein kinase C. IL-8 induction by NO was also reduced by hydroxyl radical scavengers such as dimethyl sulfoxide and dimethylthiourea, indicating the involvement of hydroxyl radicals in the induction process. NO induction of IL-8 gene expression could be a significant contributing factor in the initiation and induction of inflammatory response in the respiratory epithelium.

scholarly journals Induction of Fibrinogen Biosynthesis and Secretion From Cultured Pulmonary Epithelial Cells

Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 873-882 ◽  
Author(s):  
Patricia J. Simpson Haidaris
Keyword(s):  
Epithelial Cells ◽  
Gene Transcription ◽  
Wound Repair ◽  
Polymerase Chain Reaction Amplification ◽  
Lung Epithelial Cells ◽  
Response To Treatment ◽  
Chain Gene ◽  
Local Synthesis ◽  
Proinflammatory Mediators ◽  
Lung Epithelial

Abstract Although the liver is the primary site of fibrinogen (FBG) synthesis, epithelial cells from diverse tissues have been shown to express one or more of the FBG Aα, Bβ, and γ chain genes. In contrast, marrow megakaryocytes, which store FBG in the α-granules, are thought not to express the FBG genes. Our earlier studies have shown that epithelial cells in a variety of extrahepatic tissues express the γ chain gene ubiquitously, while the mRNAs for the Aα and Bβ chain genes are essentially undetectable. During systemic inflammation, the liver secretes increased levels of FBG into the circulation, and lung epithelium responds to local inflammation during pulmonary infection by increased transcription of the γ-FBG gene. Therefore, to determine whether extrahepatic epithelial cells express the Aα, Bβ, and γ chain genes in response to proinflammatory mediators, cultured lung epithelial cells were treated with interleukin-6 (IL-6) and dexamethasone (DEX). Northern blot analysis demonstrated that the levels of γ-FBG mRNA in cultured lung (A549) and liver (HepG2) epithelial cells increased 2- to 10-fold in response to treatment. Reverse-transcriptase-polymerase chain reaction amplification demonstrated increased accumulation of steady state levels of FBG Aα, Bβ, and γ chain mRNAs in lung epithelial cells after treatment. The basal level of lung cell γ-FBG gene transcription was not accompanied by appreciable levels of Aα and Bβ chain gene transcription; however, nuclear run-on analysis suggested that the increase in lung cell FBG mRNAs in response to DEX ± IL-6 was due to new transcription. Furthermore, stimulation of lung epithelial cells with IL-6 + DEX resulted in maximal secretion of intact FBG (340 kD) composed of the characteristic Aα, Bβ, and γ chain polypeptides. The data suggest that basal expression of the γ-FBG gene in extrahepatic tissue occurs ubiquitously in the absence of detectable levels of Aα- and Bβ-FBG gene expression, which are then upregulated on induction of an inflammatory response. This would result in local synthesis and secretion of FBG in the injured tissue, supporting the hypothesis that production of FBG by extrahepatic epithelial cells in response to inflammation plays a role in wound repair.

Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling

2006 ◽  
Vol 290 (2) ◽  
pp. L317-L325 ◽  
Author(s):  
Jesse Roman ◽  
Hilda N. Rivera ◽  
Susanne Roser-Page ◽  
Shanthi V. Sitaraman ◽  
Jeffrey D. Ritzenthaler
Keyword(s):  
Epithelial Cells ◽  
Gene Transcription ◽  
Tissue Remodeling ◽  
Lung Epithelial Cells ◽  
Lung Fibroblasts ◽  
Luciferase Reporter ◽  
Intracellular Camp ◽  
Dependent Manner ◽  
Lung Epithelial ◽  
Fibronectin Expression

Adenosine is an extracellular nucleoside that is elevated in tissues during hypoxia and ischemia reperfusion and has been implicated in asthma and other lung disorders. There, adenosine is considered an important modulator of physiological functions and inflammation, but its effects on matrix expression and turnover during tissue remodeling are unknown. We examined the effects of adenosine on lung epithelial cells with particular attention to the expression of fibronectin, a matrix glycoprotein highly expressed in injured tissues that has been implicated in wound healing. In A549 lung epithelial cells, we found that adenosine induced expression of fibronectin mRNA and protein in a dose- and time-dependent manner and found that the stimulatory effect of adenosine was inhibited by specific adenosine receptor antagonists. Adenosine stimulation was associated with increased levels of intracellular cAMP and with phosphorylation and DNA binding of the cAMP response element binding protein (CREB), known for its ability to stimulate fibronectin gene transcription. To confirm the latter, A549 cells were transfected with a DNA construct containing the human fibronectin promoter connected to a luciferase reporter gene. Adenosine stimulated transcription of the gene, and this effect was blocked by inhibitors of protein kinase activation. Finally, we tested primary lung fibroblasts and primary alveolar epithelial type II cells and found increased fibronectin expression in response to adenosine. Overall, our observations suggest that adenosine might modulate tissue remodeling by stimulating fibronectin expression in lung epithelial cells through induction of purinergic receptor-mediated signals that target CREB phosphorylation and stimulate fibronectin gene transcription.

Legionella pneumophila induced microRNA expression in human lung epithelial cells

Pneumologie ◽  
2010 ◽  
Vol 64 (S 03) ◽  
Author(s):  
B Schmeck ◽  
B Dolniak ◽  
I Pollock ◽  
C Schulz ◽  
W Bertrams ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Legionella Pneumophila ◽  
Human Lung ◽  
Microrna Expression ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

Microscopy study on the interaction of silica nanoparticles with lung epithelial cells

Pneumologie ◽  
2013 ◽  
Vol 67 (12) ◽  
Author(s):  
H Peuschel ◽  
T Ruckelshausen ◽  
C Cavelius ◽  
A Kraegeloh
Keyword(s):  
Epithelial Cells ◽  
Silica Nanoparticles ◽  
Microscopy Study ◽  
Lung Epithelial Cells ◽  
Lung Epithelial
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