Leukotriene D4 (LTD4), EGF and TGFβ Interact Synergistically to Increase The Accumulation of the Extracellular Matrix Component, Hyaluronan, in Cultured Human Lung Fibroblast Cultures (HLF)

2008 ◽  
Vol 121 (2) ◽  
pp. S121-S121
Author(s):  
P JOHNSON ◽  
S PERIGO ◽  
K BRAUN ◽  
C CHAN ◽  
L ALTMAN ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Human Lung ◽  
Lung Fibroblast ◽  
Extracellular Matrix Component ◽  
Matrix Component ◽  
Leukotriene D4 ◽  
Human Lung Fibroblast ◽  
Fibroblast Cultures

Effects of silica on human lung fibroblast in culture

2001 ◽  
Vol 270 (1-3) ◽  
pp. 135-139 ◽  
Author(s):  
G Arcangeli ◽  
V Cupelli ◽  
G Giuliano
Keyword(s):  
Human Lung ◽  
Lung Fibroblast ◽  
Human Lung Fibroblast

scholarly journals Hyperglycaemia and aberrated insulin signalling stimulate tumour progression via induction of the extracellular matrix component hyaluronan

2017 ◽  
Vol 141 (4) ◽  
pp. 791-804 ◽  
Author(s):  
Sören Twarock ◽  
Christina Reichert ◽  
Ulrike Peters ◽  
Daniel J. Gorski ◽  
Katharina Röck ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Insulin Signalling ◽  
Tumour Progression ◽  
Extracellular Matrix Component ◽  
Matrix Component

Regulation of human lung fibroblast phenotype and function by vitronectin and vitronectin integrins

2001 ◽  
Vol 114 (19) ◽  
pp. 3507-3516 ◽  
Author(s):  
Amelia K. Scaffidi ◽  
Yuben P. Moodley ◽  
Markus Weichselbaum ◽  
Philip J. Thompson ◽  
Darryl A. Knight
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Monoclonal Antibodies ◽  
Human Lung ◽  
Stress Fibers ◽  
Collagen Gels ◽  
Human Lung Fibroblast ◽  
Myofibroblast Phenotype ◽  
And Function ◽  
Blocking Antibodies

Myofibroblasts, characterised by high expression of α-smooth muscle actin (α-SMA), are important and transient cells in normal wound healing but are found in increased number in various pathological conditions of the lung including asthma and pulmonary fibrosis. The mechanisms that regulate the myofibroblast phenotype are unknown but are likely to involve signals from the extracellular matrix transmitted via specific integrins. Vitronectin is a glycoprotein released during inflammation and has been shown to regulate the phenotype of vascular smooth muscle cells via αv and β1 integrins. In the current study we have examined whether vitronectin influences the phenotype and function of normal human lung fibroblasts (HFL-1). Incubation of HFL-1 cells with vitronectin induced a concentration-dependent reduction in α-SMA expression. By contrast, function-blocking monoclonal antibodies to the vitronectin integrins αv, β1, αvβ3 and αvβ5 induced the expression of α-SMA and its organization into stress fibers. Expression of α-SMA induced by all function-blocking monoclonal antibodies was abrogated by inhibition of protein kinase C and phosphatidylinositol-3 kinase, but the effects of inhibition of other signalling pathways was integrin dependent. Exposure to other extracellular matrix proteins such as fibronectin, collagen or their integrins did not influence expression of α-SMA. The expression and organization of α-SMA induced by exposure to function-blocking antibodies was translated into an augmented capacity of HFL-1 cells to contract fibroblast populated collagen gels. By contrast, contraction of collagen gels following incubation with vitronectin was not significantly different to control. This study has shown that vitronectin influences the phenotype and behaviour of HFL-1 cells by downregulating the expression of α-SMA and reducing their contractile ability. By contrast, occupancy of specific integrins by function-blocking antibodies upregulated the expression of α-SMA and induced the formation of functional stress fibers capable of contracting collagen gels. These results suggest that vitronectin modulates the fibroblast-myofibroblast phenotype, implying an important role in the remodelling process during lung development or response to injury.

Surfactant downregulates synthesis of DNA and inflammatory mediators in normal human lung fibroblasts

1996 ◽  
Vol 270 (1) ◽  
pp. L159-L163 ◽  
Author(s):  
M. J. Thomassen ◽  
J. M. Antal ◽  
B. P. Barna ◽  
L. T. Divis ◽  
D. P. Meeker ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Human Lung ◽  
Thymidine Incorporation ◽  
Interleukin 1 ◽  
S Phase ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblast ◽  
Normal Human

The initial inflammatory event in the adult respiratory distress syndrome (ARDS) is followed by fibroproliferation and a cascade of fibroblast-derived mediators. Because lung fibroblasts may be exposed to surfactant as well as inflammatory cytokines during ARDS, we hypothesized that surfactant might modulate fibroblast activity. We previously demonstrated that surfactant inhibited production of inflammatory cytokines from endotoxin-stimulated human alveolar macrophages. In the current study the effects of surfactant on normal human lung fibroblast proliferative capacity and mediator production were examined. Both synthetic (Exosurf) and natural (Survanta) surfactant inhibited fibroblast [3H]thymidine incorporation. Examination of pre-S-phase events indicated stimulation of the immediate response gene, c-fos, and no effect on the G1/S cyclin, cyclin D1, suggesting that the surfactant block occurred elsewhere before S phase. The antioxidant N-acetyl-L-cysteine (NAC), like surfactant, inhibited [3H]thymidine incorporation. Furthermore, menadione, a generator of intracellular H2O2, stimulated fibroblast [3H]thymidine incorporation, and this was inhibited by surfactant. Interleukin-1 (IL-1)-stimulated secretion of the inflammatory mediators, IL-6 and prostaglandin E2, was also inhibited by surfactant. These data suggest that surfactant may modify lung fibroblast participation in ARDS sequelae by downregulating DNA synthesis and secondary inflammatory mediator production.

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