Collagen secretion mediated by NMDR activation in human fetal lung fibroblasts

2010 ◽  
Vol 34 (8) ◽  
pp. S70-S70
Author(s):  
MingJie WANG ◽  
ZiQiang LUO ◽  
Mei LU ◽  
LiHong SHANG ◽  
ShaoJie YUE
Keyword(s):  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Collagen Secretion ◽  
Human Fetal Lung

scholarly journals MORPHOGENETIC ASPECTS OF MULTILAYERING IN PETRI DISH CULTURES OF HUMAN FETAL LUNG FIBROBLASTS

1969 ◽  
Vol 41 (1) ◽  
pp. 298-311 ◽  
Author(s):  
Tom Elsdale ◽  
Robert Foley
Keyword(s):  
Extracellular Matrix ◽  
Human Lung ◽  
Petri Dish ◽  
Fetal Lung ◽  
Single Species ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblasts ◽  
Spontaneous Aggregation ◽  
Control Hypothesis ◽  
Human Fetal Lung

Randomly seeded Petri dish cultures of embryonic human lung fibroblasts generate, in the course of their growth, highly ordered cellular arrangements. Thick, bilaterally symmetrical ridges with an axial polarity and an orthogonal, multilayered internal organization are observed within stationary cultures. The generation of these structures has been investigated. Ridges result from the spontaneous aggregation of cells in postconfluent cultures brought about by directed cell movements. These movements are promoted by the localized production of extracellular matrix sheets containing collagen, which provide new substrates for cellular colonization. Cells that have colonized one matrix substrate may secrete another above themselves, which will in turn be colonized. By a continuation of this cycle, thick stacks consisting of alternate layers of cells and matrix are produced to yield the observed aggregations. The distribution and shape of ridges in a culture imply that matrix substrates are confined to specific locations. The suggested control hypothesis assumes that all the cells in fibroblast cultures are potential producers of a single species of matrix. The serviceability of this matrix as a substrate for cellular colonization, however, is destroyed if the producer cells are motile. Matrix substrates, therefore, are only made by nonmotile cells.

Prostacyclin analogs inhibit fibroblast migration

2002 ◽  
Vol 283 (2) ◽  
pp. L428-L432 ◽  
Author(s):  
Tadashi Kohyama ◽  
Xiangde Liu ◽  
Hui Jung Kim ◽  
Tetsu Kobayashi ◽  
Ronald F. Ertl ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Fetal Lung ◽  
Inhibitory Effect ◽  
Lung Fibroblasts ◽  
Fibroblast Migration ◽  
Inflammatory Processes ◽  
Dependent Protein ◽  
Pka Pathway ◽  
Human Fetal Lung ◽  
Abnormal Tissue

The controlled accumulation of fibroblasts to sites of inflammation is crucial to effective tissue repair after injury. Either inadequate or excessive accumulation of fibroblasts could result in abnormal tissue function. Prostacyclin (PGI2) is a potent mediator in the coagulation and inflammatory processes. The aim of this study was to investigate the effect of PGI2on chemotaxis of human fetal lung fibroblasts (HFL-1). Using the blind well chamber technique, we found that the PGI2analog carbaprostacyclin (10−6M) inhibited HFL-1 chemotaxis to human plasma fibronectin (20 μg/ml) 58.0 ± 13.2% ( P < 0.05) and to platelet-derived growth factor (PDGF)-BB (10 ng/ml) 48.7 ± 4.6% ( P < 0.05). Checkerboard analysis demonstrated that carbaprostacyclin inhibits both directed and undirected migration. The inhibitory effect of the carbaprostacyclin was concentration dependent and blocked by the cAMP-dependent protein kinase (PKA) inhibitor KT-5720, suggesting that a cAMP-PKA pathway may be involved in the process. Two other PGI2analogs, ciprostene and dehydro-15-cyclohexyl carbaprostacyclin (both 10−6M), significantly inhibited fibroblast migration to fibronectin. In summary, PGI2appears to inhibit fibroblast chemotaxis to fibronectin and PDGF-BB. Such an effect may contribute to the regulation of fibroblasts in wound healing and could contribute to the pathogenesis of diseases characterized by abnormal tissue repair remodeling.

Collagen glucosyl- and galactosyltransferases of cultured human fetal lung fibroblasts

1981 ◽  
Vol 210 (2) ◽  
pp. 678-690 ◽  
Author(s):  
Hilda H. Carnicero ◽  
Anthony M. Adamany ◽  
Sasha Englard
Keyword(s):  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Human Fetal Lung

scholarly journals Loss of FLCN inhibits canonical WNT signaling via TFE3

2019 ◽  
Vol 28 (19) ◽  
pp. 3270-3281 ◽  
Author(s):  
John C Kennedy ◽  
Damir Khabibullin ◽  
Thomas Hougard ◽  
Julie Nijmeh ◽  
Wei Shi ◽  
...  
Keyword(s):  
Wnt Pathway ◽  
Lower Lobe ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Pulmonary Cysts ◽  
Wnt Ligands ◽  
Neonatal Lung ◽  
Canonical Wnt ◽  
Human Fetal Lung ◽  
Bhd Syndrome

Abstract Lower lobe predominant pulmonary cysts occur in up to 90% of patients with Birt–Hogg–Dubé (BHD) syndrome, but the key pathologic cell type and signaling events driving this distinct phenotype remain elusive. Through examination of the LungMAP database, we found that folliculin (FLCN) is highly expressed in neonatal lung mesenchymal cells. Using RNA-Seq, we found that inactivation of Flcn in mouse embryonic fibroblasts leads to changes in multiple Wnt ligands, including a 2.8-fold decrease in Wnt2. This was associated with decreased TCF/LEF activity, a readout of canonical WNT activity, after treatment with a GSK3-α/β inhibitor. Similarly, FLCN deficiency in HEK293T cells decreased WNT pathway activity by 76% post-GSK3-α/β inhibition. Inactivation of FLCN in human fetal lung fibroblasts (MRC-5) led to ~ 100-fold decrease in Wnt2 expression and a 33-fold decrease in Wnt7b expression—two ligands known to be necessary for lung development. Furthermore, canonical WNT activity was decreased by 60%. Classic WNT targets such as AXIN2 and BMP4, and WNT enhanceosome members including TCF4, LEF1 and BCL9 were also decreased after GSK3-α/β inhibition. FLCN-deficient MRC-5 cells failed to upregulate LEF1 in response to GSK3-α/β inhibition. Finally, we found that a constitutively active β-catenin could only partially rescue the decreased WNT activity phenotype seen in FLCN-deficient cells, whereas silencing the transcription factor TFE3 completely reversed this phenotype. In summary, our data establish FLCN as a critical regulator of the WNT pathway via TFE3 and suggest that FLCN-dependent defects in WNT pathway developmental cues may contribute to lung cyst pathogenesis in BHD.

Ammonium chloride inhibits basal degradation of newly synthesized collagen in human fetal lung fibroblasts

1990 ◽  
Vol 276 (1) ◽  
pp. 125-131 ◽  
Author(s):  
Frank A. Barile ◽  
Dorothy E. Guzowski ◽  
Catherine Ripley ◽  
Zafar-e-Alam Siddiqi ◽  
Robert S. Bienkowski
Keyword(s):  
Ammonium Chloride ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Human Fetal Lung

Thrombin regulation of tissue-type plasminogen activator synthesis in cultured human fetal lung fibroblasts

1993 ◽  
Vol 71 (6) ◽  
pp. 457-465 ◽  
Author(s):  
Yumiko Hayakawa ◽  
Shigeki Tazawa ◽  
Tai-ichi Ishikawa ◽  
Kenji Niiya ◽  
Nobuo Sakuragawa
Keyword(s):  
Plasminogen Activator ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Human Fetal Lung

The excitotoxity of NMDA receptor NR2D subtype mediates human fetal lung fibroblasts proliferation and collagen production

2018 ◽  
Vol 46 ◽  
pp. 47-57 ◽  
Author(s):  
MingJie Wang ◽  
ZiQiang Luo ◽  
Yinyan Yue ◽  
YanRui Wang ◽  
Shu Wu ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Fetal Lung ◽  
Lung Fibroblasts ◽  
Collagen Production ◽  
Human Fetal Lung
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