scholarly journals Inhibitory effect of anti-aminopeptidase N/CD13 antibodies on fibroblast migration

2010 ◽  
Vol 343 (1-2) ◽  
pp. 191-199 ◽  
Author(s):  
Amy Lai ◽  
Abdi Ghaffari ◽  
Aziz Ghahary
Keyword(s):  
Inhibitory Effect ◽  
Aminopeptidase N ◽  
Fibroblast Migration

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.

scholarly journals Effect of heparin and related glycosaminoglycan on PDGF-induced lung fibroblast proliferation, chemotactic response and matrix metalloproteinases activity

2000 ◽  
Vol 9 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Masahiro Sasaki ◽  
Masayuki Kashima ◽  
Takefumi Ito ◽  
Akiko Watanabe ◽  
Masaaki Sano ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Human Lung ◽  
Heparan Sulphate ◽  
Inhibitory Effect ◽  
Lung Fibroblast ◽  
Chemotactic Response ◽  
Fibroblast Proliferation ◽  
Human Lung Fibroblast ◽  
Fibroblast Migration

Fibroblast migration, proliferation, extacellular matrix protein synthesis and degradation are the key events in various biological and pathological processes in pulmonary fibrosis. In addition, biopsy specimens from the lungs of patients with plumomary fibrosis show increased numbers of mast cells which have metachromatic granules containing heparin, histamin and proteases. Little is known about how these products influence pulmonary fibrosis. In the present study, we investigated the effect of heparin and related glycosaminoglycans on PDGF-induced lung fibroblast proliferation and chemotactic responsein vitro. In addition, we examined the effect of heparin on both the induction of matorix metalloproteinases (MMPs) and MMPs activity in lung fibroblastsin vitro.Heparin, de-N-sulphated heparin but not heparan sulphate inhibited PDGF-induced lung fibroblast proliferation. In contrast, only heparin inhibited PDGF-stimulated human lung fibroblast chemotaxis. Negatively charged poly-L-gultamic acid had no effect on either fibroblast proliferation or chemotaxis. Thus the negative charge alone cannot account for the ant-proliferative and anti-chemotactic effects of heparin.Furthermore, heparin and heparan sulphate also had no inhibitory effect on induction of MMPs, including MMP-1 (interstitial collagenase), MMP-2 (gelatinase A) and MMP-9 (gelatinase B). Only heparin inhibited both MMP-1 and MMP-2/MMP-9 activity. Additionally, tissue inhibitor of metalloproteinase type 1 (TIMP-1) and type 2 (TIMP-2) inhibited PDGF-stimulated human lung fibroblast chemotaxis. The ability of heparin to inhibit fibroblast chemotaxis may account for the inhibitory effect of heparin on MMP activity.The above results suggested that heparin and related glycosaminoglycans differentially regulate PDGF-induced lung fibroblast proliferation, chemotaxis and MMPs activity and further that these effects may have a key role in extracellular matrix remodeling in inflammatory lung disease.

Inhibitory effect of lycopene on PDGF-BB-induced signalling and migration in human dermal fibroblasts: a possible target for cancer

2007 ◽  
Vol 35 (5) ◽  
pp. 1377-1378 ◽  
Author(s):  
W.-B. Wu ◽  
H.-S. Chiang ◽  
J.-Y. Fang ◽  
C.-F. Hung
Keyword(s):  
Growth Factor ◽  
Stromal Cells ◽  
Cell Cycle Progression ◽  
Tumour Progression ◽  
Inflammatory Cells ◽  
Inhibitory Effect ◽  
Tumour Cells ◽  
Dermal Fibroblasts ◽  
Fibroblast Migration ◽  
Signalling Transduction

Tumours are complex tissues composed of both matrix proteins and stromal cells such as fibroblasts and inflammatory cells. Tumour progression is often the result of dynamic interactions between the tumour cells and their surroundings. Lycopene, a natural carotenoid that is abundant in tomato, has been shown to inhibit proliferation of several types of cancer cells through arrest of tumour cell-cycle progression, IGF-1 (insulin-like growth factor 1) signalling transduction, induction of apoptosis etc. However, in our recent study, we found that lycopene inhibited PDGF-BB (platelet-derived growth factor-BB)-induced signalling and cell migration in human cultured skin fibroblasts through a novel mechanism of action, i.e. direct binding to PDGF-BB. Trapping of PDGF by lycopene also compromised melanoma-induced fibroblast migration and attenuated signalling transduction in fibroblasts simulated by melanoma-derived conditioned medium, suggesting that lycopene may interfere with tumour–stroma interactions. The trapping activity of lycopene on PDGF suggests that it may act as an inhibitor on stromal cells, tumour cells and their interactions, which may contribute to its anti-tumour activity.

Prostaglandin E2 inhibits fibroblast chemotaxis

2001 ◽  
Vol 281 (5) ◽  
pp. L1257-L1263 ◽  
Author(s):  
Tadashi Kohyama ◽  
Ronald F. Ertl ◽  
Vincenzo Valenti ◽  
John Spurzem ◽  
Masashi Kawamoto ◽  
...  
Keyword(s):  
Fetal Lung ◽  
Bronchial Epithelial Cell ◽  
Inhibitory Effect ◽  
Lung Fibroblasts ◽  
Prostaglandin E ◽  
Fibroblast Migration ◽  
Wound Healing Response ◽  
Dependent Protein ◽  
Connective Tissue Matrix ◽  
Tissue Matrix

Fibroblasts are the major source of extracellular connective tissue matrix, and the recruitment, accumulation, and stimulation of these cells are thought to play important roles in both normal healing and the development of fibrosis. Prostaglandin E2(PGE2) can inhibit this process by blocking fibroblast proliferation and collagen production. The aim of this study was to investigate the inhibitory effect of PGE2 on human plasma fibronectin (hFN)- and bovine bronchial epithelial cell-conditioned medium (BBEC-CM)-induced chemotaxis of human fetal lung fibroblasts (HFL1). Using the Boyden blind well chamber technique, PGE2(10−7 M) inhibited chemotaxis to hFN 40.8 ± 5.3% ( P < 0.05) and to BBEC-CM 49.7 ± 11.7% ( P < 0.05). Checkerboard analysis demonstrated inhibition of both chemotaxis and chemokinesis. The effect of PGE2 was concentration dependent, and the inhibitory effect diminished with time. Other agents that increased fibroblast cAMP levels, including isoproterenol (10−5 M), dibutyryl cAMP (10−5 M), and forskolin (3 × 10−5 M) had similar effects and inhibited chemotaxis 54.1, 95.3, and 87.0%, respectively. The inhibitory effect of PGE2 on HFL1 cell chemotaxis was inhibited by the cAMP-dependent protein kinase (PKA) inhibitor KT-5720, which suggests a cAMP-dependent effect mediated by PKA. In summary, PGE2 appears to inhibit fibroblast chemotaxis, perhaps by modulating the rate of fibroblast migration. Such an effect may contribute to regulation of the wound healing response after injury.

Biological and biomedical applications of collagenous biomaterials

1990 ◽  
Vol 48 (3) ◽  
pp. 856-857
Author(s):  
Yasushi P. Kato ◽  
Michael G. Dunn ◽  
Frederick H. Silver ◽  
Arthur J. Wasserman
Keyword(s):  
Biomedical Applications ◽  
Soft Tissues ◽  
Collagen Fibers ◽  
Bone Collagen ◽  
Cover Slip ◽  
Fibroblast Migration ◽  
Cellular Expression ◽  
Defect Repair

Collagenous biomaterials have been used for growing cells in vitro as well as for augmentation and replacement of hard and soft tissues. The substratum used for culturing cells is implicated in the modulation of phenotypic cellular expression, cellular orientation and adhesion. Collagen may have a strong influence on these cellular parameters when used as a substrate in vitro. Clinically, collagen has many applications to wound healing including, skin and bone substitution, tendon, ligament, and nerve replacement. In this report we demonstrate two uses of collagen. First as a fiber to support fibroblast growth in vitro, and second as a demineralized bone/collagen sponge for radial bone defect repair in vivo.For the in vitro study, collagen fibers were prepared as described previously. Primary rat tendon fibroblasts (1° RTF) were isolated and cultured for 5 days on 1 X 15 mm sterile cover slips. Six to seven collagen fibers, were glued parallel to each other onto a circular cover slip (D=18mm) and the 1 X 15mm cover slip populated with 1° RTF was placed at the center perpendicular to the collagen fibers. Fibroblast migration from the 1 x 15mm cover slip onto and along the collagen fibers was measured daily using a phase contrast microscope (Olympus CK-2) with a calibrated eyepiece. Migratory rates for fibroblasts were determined from 36 fibers over 4 days.

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase

Inhibitory effect of proton pump inhibitors against chemotaxis of Helicobacter pylori

2001 ◽  
Vol 120 (5) ◽  
pp. A655-A656
Author(s):  
H NAKAMURA ◽  
H YOSHIYAMA ◽  
H YANAI ◽  
M SHIRAL ◽  
T NAKAZAWA ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Inhibitory Effect

The Nature of the Inhibitory Effect of Normal Human Gastric Jiuice on Heidenhain Pouch Dogs

1958 ◽  
Vol 34 (2) ◽  
pp. 181-187 ◽  
Author(s):  
William O. Smith ◽  
Robert Hoke ◽  
Jerome Landy ◽  
Ranwel Caputto ◽  
Stewart Wolf
Keyword(s):  
Inhibitory Effect ◽  
Heidenhain Pouch ◽  
Normal Human
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