scholarly journals microRNA‐30a attenuates TGF‐β1–induced activation of pulmonary fibroblast cell by targeting FAP‐α

2020 ◽  
Vol 24 (6) ◽  
pp. 3745-3750 ◽  
Author(s):  
Geting Wu ◽  
Bin Xie ◽  
Can Lu ◽  
Chen Chen ◽  
Jianhua Zhou ◽  
...  
Keyword(s):  
Fibroblast Cell ◽  
Pulmonary Fibroblast ◽  
Tgf Β1

Enhancement of gallic acid-induced human pulmonary fibroblast cell death by N-acetyl cysteine and L-buthionine sulfoximine

2010 ◽  
Vol 30 (8) ◽  
pp. 992-999 ◽  
Author(s):  
Bo Ra You ◽  
Woo Hyun Park
Keyword(s):  
Cell Death ◽  
Growth Inhibition ◽  
Gallic Acid ◽  
Buthionine Sulfoximine ◽  
Fibroblast Cell ◽  
Biological Properties ◽  
Dependent Manner ◽  
Toxicological Effect ◽  
Acetyl Cysteine ◽  
Pulmonary Fibroblast

Gallic acid (GA) has various biological properties including anti-cancer effect. However, little is known about the toxicological effect of GA in primary normal cells. Here, we evaluated the effects of GA on human pulmonary fibroblast (HPF) cells in relation to reactive oxygen species (ROS) and glutathione (GSH). GA inhibited the growth of HPF cells at 24 hours in a dose-dependent manner. GA also induced HPF cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; ΔΨm). GA increased ROS levels including O2•- and GSH-depleted cell numbers in HPF cells at 24 hours. Treatment with 2 mM N-acetyl-cysteine (NAC) intensified growth inhibition and death in GA-treated HPF cells. NAC decreased ROS levels and increased GSH depletion in these cells. Treatment with 10 μM L-buthionine sulfoximine (BSO) also enhanced growth inhibition and death in GA-treated HPF cells. BSO increased ROS levels and GSH depletion in these cells. In conclusion, GA-induced HPF cell death was accompanied by ROS increase and GSH depletion. The changes of ROS and GSH levels by NAC and BSO appeared to affect cell growth and death in GA-treated HPF cells.

TGF-β1 Modulates HGF/SF in Keloid Fibroblast Cell Culture

2008 ◽  
Vol 139 (2_suppl) ◽  
pp. P32-P33 ◽  
Author(s):  
Ramin Naim ◽  
Andreas Naumann ◽  
James Barnes ◽  
Alexander Sauter ◽  
Karl Hormann ◽  
...  
Keyword(s):  
Cell Culture ◽  
Wound Healing ◽  
Antisense Oligonucleotides ◽  
Fibroblast Cell ◽  
Neutralising Antibodies ◽  
Keloid Fibroblast ◽  
Keloid Formation ◽  
Fibroblast Cell Culture ◽  
Or Gene ◽  
Tgf Β1

Objective Abnormal wound healing processes can result in hypertrophic scars and keloids. TGF-β1 and HGF/SF are biphasic growth factor cytokines in physiological and pathophysiological conditions. TGF-β1 has been found to be pivotal in the formation of keloid tissue and therefore neutralising antibodies may allow wound healing without keloid formation. TGF-β1 has been reported to be antagonised by HGF/SF. Some authors have reported that exogenous administration of HGF/SF prevented scar formation. Hence in this study, we targeted TGF-β1 and determined the levels of HGF/SF in fibroblast cell culture. Methods Keloid tissue was taken from 7 patients while another 7 patients with mature non-hypertrophic scar served as controls. All tissues were cultured and fibroblast cultures were used for further experiments. TGF-β1 antisense was administered at 3 and 6 μmol/ml and HGF/SF levels were determined after 16, 24 and 48 hours of incubation. Results The levels of HGF/SF showed significant differences after incubation with antisense oligonucleotides. The increasing antisense levels resulted in increased HGF/SF levels (up to 87.66pg/ml after 48 hours of incubation). Conclusions In conclusion, targeting TGF-β1 resulted in significantly increased levels of HGF/SF. The clinical relevance could include the use of locally administered HGF/SF in protein or gene form to minimise keloid formation. Nevertheless, wound healing is the result of many interacting cytokines and therefore neutralising or targeting one protein could result in no significant effect.

GRK2 promotes activation of lung fibroblast cells and contributes to pathogenesis of pulmonary fibrosis through increasing Smad3 expression

2021 ◽  
Author(s):  
Yanhui Li ◽  
Ying Sun ◽  
Nan Wu ◽  
Haichun Ma
Keyword(s):  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Fibroblast Cell ◽  
Cell Types ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Fibroblast Cells ◽  
Smad3 Expression ◽  
Tgf Β1

Pulmonary fibrosis is a chronic, progressive, and irreversible interstitial lung disease. Transforming growth factor beta1 (TGF-β1) plays a major role in lung fibroblast cell differentiation to myofibroblast cells and production of extracellular matrix, which are hallmarks of pulmonary fibrosis. G protein-coupled receptor kinase-2 (GRK2) has been shown to play controversial roles in TGF-β1-induced signal transduction in different cell types; however, the roles of GRK2 in TGF-β1-induced activation of lung fibroblast cells and development of pulmonary fibrosis have not been revealed. In this study, we found that GRK2 levels were induced in lungs and isolated fibroblast cells in a murine model of pulmonary fibrosis, as well as TGF-β1-treated lung fibroblasts. GRK2 levels were not changed in lungs in the injury phase of pulmonary fibrosis. Post-treatment with GRK2 inhibitor reduced ECM accumulation in lungs in bleomycin-challenged mice, suggesting that GRK2 activation contributes to the progressive phase of pulmonary fibrosis. Inhibition or downregulation of GRK2 attenuates fibronectin, collagen, and α-smooth muscle actin expression in TGF-β1-induced lung fibroblast cells or myofibroblast cells isolated from pulmonary fibrosis patients. Further, we showed that GRK2 regulates Smad3 expression, indicating that inhibition of GRK2 attenuates ECM accumulation through downregulation of Smad3 expression. This study reveals that GRK2 is a therapeutic target in treating pulmonary fibrosis and inhibition of GRK2 dampens pulmonary fibrosis by suppression of Smad3 expression, eventually attenuating TGF-β1 signal pathway and ECM accumulation.

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