Ultrafine Carbon Black Particles Inhibit Human Lung Fibroblast-Mediated Collagen Gel Contraction

2003 ◽  
Vol 28 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Huijung Kim ◽  
Xiangde Liu ◽  
Tetsu Kobayashi ◽  
Tadashi Kohyama ◽  
Fu-Qiang Wen ◽  
...  
Keyword(s):  
Carbon Black ◽  
Human Lung ◽  
Collagen Gel ◽  
Lung Fibroblast ◽  
Human Lung Fibroblast ◽  
Collagen Gel Contraction

Sodium nitroprusside augments human lung fibroblast collagen gel contraction independently of NO-cGMP pathway

2000 ◽  
Vol 278 (5) ◽  
pp. L1032-L1038 ◽  
Author(s):  
X. D. Liu ◽  
C. M. Skold ◽  
T. Umino ◽  
J. R. Spurzem ◽  
D. J. Romberger ◽  
...  
Keyword(s):  
Type I Collagen ◽  
Human Lung ◽  
Three Dimensional ◽  
Collagen Gel ◽  
Lung Fibroblast ◽  
Type I ◽  
Collagen Gels ◽  
Human Lung Fibroblast ◽  
Collagen Gel Contraction ◽  
Cgmp Pathway

Nitric oxide (NO) relaxes vascular smooth muscle in part through an accumulation of cGMP in the target cells. We hypothesized that a similar effect may also exist on collagen gel contraction mediated by human fetal lung (HFL1) fibroblasts, a model of wound contraction. To evaluate this, HFL1 cells were cultured in three-dimensional type I collagen gels and floated in serum-free DMEM with and without various NO donors. Gel size was measured with an image analyzer. Sodium nitroprusside (SNP, 100 μM) significantly augmented collagen gel contraction by HFL1 cells (78.5 ± 0.8 vs. 58.3 ± 2.1, P < 0.01), whereas S-nitroso- N-acetylpenicillamine, 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium chloride, NONOate, and N G-monomethyl-l-arginine did not affect the contraction. Sodium ferricyanide, sodium nitrate, or sodium nitrite was not active. The augmentory effect of SNP could not be blocked by 1 H-[1,2,4]-oxadiazolo-[4,3- a]-quinoxalin-1-one, whereas it was partially reversed by 8-(4-chlorophenylthio) (CPT)-cGMP. To further explore the mechanisms by which SNP acted, fibronectin and PGE2 production were measured by immunoassay after 2 days of gel contraction. SNP inhibited PGE2 production and increased fibronectin production by HFL1 cells in a concentration-dependent manner. CPT-cGMP had opposite effects on fibronectin and PGE2 production. Addition of exogenous PGE2 blocked SNP-augmented contraction and fibronectin production by HFL1 cells. Therefore, SNP was able to augment human lung fibroblast-mediated collagen gel contraction, an effect that appears to be independent of NO production and not mediated through cGMP. Decreased PGE2 production and augmented fibronectin production may have a role in this effect. These data suggest that human lung fibroblasts in three-dimensional type I collagen gels respond distinctly to SNP by mechanisms unrelated to the NO-cGMP pathway.

Histamine induces human lung fibroblast-mediated collagen gel contraction via histamine H1 receptor

2014 ◽  
Vol 40 (5) ◽  
pp. 222-236 ◽  
Author(s):  
Masafumi Horie ◽  
Akira Saito ◽  
Yasuhiro Yamauchi ◽  
Yu Mikami ◽  
Makiko Sakamoto ◽  
...  
Keyword(s):  
Human Lung ◽  
Collagen Gel ◽  
Lung Fibroblast ◽  
H1 Receptor ◽  
Human Lung Fibroblast ◽  
Histamine H1 Receptor ◽  
Collagen Gel Contraction

scholarly journals PGE2Desensitizesβ-Agonist Effect on Human Lung Fibroblast-Mediated Collagen Gel Contraction through Upregulating PDE4

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Qiuhong Fang ◽  
Yingmin Ma ◽  
Jing Wang ◽  
Joel Michalski ◽  
Stephen I. Rennard ◽  
...  
Keyword(s):  
Human Lung ◽  
Collagen Gel ◽  
Inhibitory Effect ◽  
Lung Fibroblast ◽  
Lung Fibroblasts ◽  
Pde4 Inhibitor ◽  
Dependent Manner ◽  
Human Lung Fibroblast ◽  
Collagen Gel Contraction ◽  
Long Acting

In the current study, we investigated the effect of a long-actingβ-agonist (salmeterol) and a phosphodiesterase 4 (PDE4) inhibitor (cilomilast) on human lung fibroblast-mediated collagen gel contraction. Higher concentrations of salmeterol (10−7and 10−6 M) inhibited fibroblast-mediated collagen gel contraction. No effect was observed with cilomilast alone (up to 10−5 M). In the presence of 10−8 M salmeterol, however, cilomilast could significantly inhibit fibroblast-mediated collagen gel contraction in a concentration-dependent manner (10−7~10−5 M). Blockade of endogenous PGE2by indomethacin further potentiated the inhibitory effect of salmeterol on fibroblast-mediated collagen gel contraction, but it did not affect cilomilast's effect. Pretreatment with PGE2abolished the inhibitory effect of salmeterol, but it potentiated the inhibitory effect of cilomilast on fibroblast-mediated collagen gel contraction. Finally, indomethacin slightly inhibited PDE4C expression, while PGE2stimulated the expression of PDE4A and -4C in human lung fibroblasts. These findings suggest that long-actingβ-agonist and PDE4 inhibitor have a synergistic effect in regulating fibroblast tissue repair functions and that PGE2can modulate the effect ofβ-agonist and PDE4 inhibitor at least in part through the mechanism of regulating PDE4 expression.

In vitro cytotoxicity of carbon black nanoparticles synthesized from solution plasma on human lung fibroblast cells

2017 ◽  
Vol 57 (1) ◽  
pp. 0102BG ◽  
Author(s):  
Gasidit Panomsuwan ◽  
Chayanaphat Chokradjaroen ◽  
Ratana Rujiravanit ◽  
Tomonaga Ueno ◽  
Nagahiro Saito
Keyword(s):  
Carbon Black ◽  
Human Lung ◽  
In Vitro Cytotoxicity ◽  
Lung Fibroblast ◽  
Fibroblast Cells ◽  
Human Lung Fibroblast ◽  
Carbon Black Nanoparticles

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
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