scholarly journals Simple Devices to Facilitate the Analysis of Collagen Contraction by Cells

BioTechniques ◽  
2000 ◽  
Vol 29 (3) ◽  
pp. 412-418 ◽  
Author(s):  
Arno W. Tilles ◽  
Jeanne M. Classen ◽  
Mehmet Toner ◽  
Livingston Van De Water
Keyword(s):  
Collagen Contraction

scholarly journals TGF-β1 Activates Nasal Fibroblasts through the Induction of Endoplasmic Reticulum Stress

Biomolecules ◽  
2020 ◽  
Vol 10 (6) ◽  
pp. 942
Author(s):  
Jae-Min Shin ◽  
Ju-Hyung Kang ◽  
Joo-Hoo Park ◽  
Hyun-Woo Yang ◽  
Heung-Man Lee ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Inflammatory Diseases ◽  
Upper Airway ◽  
Tissue Remodeling ◽  
Organ Cultures ◽  
Stress Marker ◽  
Stress Markers ◽  
Collagen Contraction ◽  
Tgf Β1

(1) Background: Tissue remodeling and extracellular matrix (ECM) accumulation contribute to the development of chronic inflammatory diseases of the upper airway. Endoplasmic reticulum (ER) stress is considered to be the key signal for triggering tissue remodeling in pathological conditions. The present study aimed to investigate the role of ER-stress in TGF-β1-stimulated nasal fibroblasts and inferior turbinate organ cultures; (2) Methods: Fibroblasts and organ cultures were pretreated with 4-phenylbutyric acid (PBA) and stimulated with TGF-β1 or thapsigargin (TG). Expression of ER-stress markers, myofibroblast marker, and ECM components was measured by Western blotting and real-time PCR. Reactive oxygen species (ROS) were quantified using 2′,7′-dichlorofluorescein diacetate. Cell migration was evaluated using Transwell assays. Contractile activity was measured by collagen contraction assay; (3) Results: 4-PBA inhibited TGF-β1 or TG-induced ER-stress marker expression, phenotypic changes, and ECM. Pre-treatment with ROS scavengers inhibited the expression of TGF-β1-induced ER-stress markers. Migration and collagen contraction of TGF-β1 or TG-stimulated fibroblasts were ameliorated by 4-PBA treatment. These findings were confirmed in ex vivo organ cultures; (4) Conclusions: 4-PBA downregulates TGF-β1-induced ER-stress marker expression, migration, and collagen contraction via ROS in fibroblasts and organ cultures. These results suggest that ER-stress may play an important role in progression of chronic upper airway inflammatory diseases by aiding pathological tissue remodeling.

scholarly journals Modulation of cutaneous extracellular collagen contraction by phosphorylation status of p130Cas

2016 ◽  
Vol 67 (5) ◽  
pp. 613-622 ◽  
Author(s):  
Mayumi Takeya ◽  
Yuushi Okumura ◽  
Takeshi Nikawa
Keyword(s):  
Collagen Contraction

scholarly journals An Oenothera biennis Cell Cultures Extract Endowed with Skin Anti-Ageing Activity Improves Cell Mechanical Properties

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 527
Author(s):  
Sara Ceccacci ◽  
Adriana De Lucia ◽  
Annalisa Tito ◽  
Assunta Tortora ◽  
Danila Falanga ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Actin Polymerization ◽  
Ex Vivo ◽  
Skin Aging ◽  
Point Of View ◽  
Elastic Fibers ◽  
Oenothera Biennis ◽  
Contraction Process ◽  
Collagen Contraction

Skin aging is a very well-known process setting a gradual worsening of skin mechanical features due to a decline in the production of the extra-cellular matrix machinery and to a concurrent change in the contraction process. To slow this progression, it is crucial to induce the expression of several proteins able to promote elastic fibers formation and tissue repair. Here, the Oenothera biennis cell culture aqueous extract has been investigated from a chemical point of view and then it was tested in vitro, in cell, and in ex vivo experiments as adjuvant in counteracting skin aging. Accordingly, it has been shown that the Oenothera biennis extract was able, by increasing MYLK gene expression, to promote matrix collagen contraction, actin polymerization, and the production of essential ECM proteins.

scholarly journals AR12286 Alleviates TGF-β-Related Myofibroblast Transdifferentiation and Reduces Fibrosis after Glaucoma Filtration Surgery

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4422
Author(s):  
Wen-Sheng Cheng ◽  
Ching-Long Chen ◽  
Jiann-Torng Chen ◽  
Le-Tien Lin ◽  
Shu-I Pao ◽  
...  
Keyword(s):  
Cell Migration ◽  
Intraocular Pressure ◽  
Kinase Inhibitor ◽  
Control Group ◽  
Filtration Surgery ◽  
Glaucoma Filtration Surgery ◽  
Collagen Contraction ◽  
Β Receptor ◽  
Tgf Β1

Scar formation can cause the failure of glaucoma filtration surgery. We investigated the effect of AR12286, a selective Rho-associated kinase inhibitor, on myofibroblast transdifferentiation and intraocular pressure assessment in rabbit glaucoma filtration surgery models. Cell migration and collagen contraction were used to demonstrate the functionality of AR12286-modulated human conjunctival fibroblasts (HConFs). Polymerase chain reaction quantitative analysis was used to determine the effect of AR12286 on the production of collagen Type 1A1 and fibronectin 1. Cell migration and collagen contraction in HConFs were activated by TGF-β1. However, compared with the control group, rabbit models treated with AR12286 exhibited higher reduction in intraocular pressure after filtration surgery, and decreased collagen levels at the wound site in vivo. Therefore, increased α-SMA expression in HConFs induced by TGF-β1 could be inhibited by AR12286, and the production of Type 1A1 collagen and fibronectin 1 in TGF-β1-treated HConFs was inhibited by AR12286. Overall, the stimulation of HConFs by TGF-β1 was alleviated by AR12286, and this effect was mediated by the downregulation of TGF-β receptor-related SMAD signaling pathways. In vivo results indicated that AR12286 thus improves the outcome of filtration surgery as a result of its antifibrotic action in the bleb tissue because AR12286 inhibited the TGF-β receptor-related signaling pathway, suppressing several downstream reactions in myofibroblast transdifferentiation.

Evidence for sequential utilization of fibronectin, vitronectin, and collagen during fibroblast-mediated collagen contraction

2002 ◽  
Vol 10 (6) ◽  
pp. 397-408 ◽  
Author(s):  
Kamaljit K. Sethi ◽  
Ioannis V. Yannas ◽  
Vivek Mudera ◽  
Mark Eastwood ◽  
Clive McFarland ◽  
...  
Keyword(s):  
Collagen Contraction

scholarly journals Establishment and transformation diminish the ability of fibroblasts to contract a native collagen gel.

1980 ◽  
Vol 87 (1) ◽  
pp. 304-308 ◽  
Author(s):  
B M Steinberg ◽  
K Smith ◽  
M Colozzo ◽  
R Pollack
Keyword(s):  
Serum Concentration ◽  
Human Fibroblasts ◽  
Collagen Gel ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Collagen Contraction ◽  
Absolute Efficiency ◽  
Sv40 Transformation ◽  
Native Collagen ◽  
Hydrated Collagen Gel

Cultures of established and transformed fibroblasts were less able to contract a hydrated collagen gel than normal precrisis cells. Postcrisis fibroblasts from different rodent strains and species underwent a further reduction in contraction ability and either spontaneous or simian virus 40 (SV40) transformation. Human precrisis fibroblasts contracted much more efficiently than two SV40-transformed human lines. Fibroblasts from a patient with Glanzmann's thrombasthenia were intermediate between all other human fibroblasts assayed and the SV40-transformed human lines. The absolute efficiency of contraction was dependent on temperature and serum concentration, but no conditions were found that resulted in equal efficiencies for the three types of cells. Precrisis cells were extremely sensitive to the passage procedures when assayed for collagen contraction.

S19.3. Collagen contraction by corneal, skin and tendon fibroblasts; Mechanisms and force effects

Biorheology ◽  
1995 ◽  
Vol 32 (2-3) ◽  
pp. 175-176
Author(s):  
B JOHNSONWINT ◽  
R GRYMES ◽  
A MALOUVIER
Keyword(s):  
Collagen Contraction

Effects of Pirfenidone on Proliferation, Migration, and Collagen Contraction of Human Tenon’s Fibroblasts In Vitro

2009 ◽  
Vol 50 (8) ◽  
pp. 3763 ◽  
Author(s):  
Xianchai Lin ◽  
Minbin Yu ◽  
Kaili Wu ◽  
Hongzhi Yuan ◽  
Hua Zhong
Keyword(s):  
Collagen Contraction

Higher TRIP-1 level explains diminished collagen contraction ability of fetal versus adult fibroblasts

2009 ◽  
Vol 296 (6) ◽  
pp. L928-L935 ◽  
Author(s):  
Angels Navarro ◽  
Mo Rezaiekhaligh ◽  
J. Andrew Keightley ◽  
Sherry M. Mabry ◽  
Ricardo E. Perez ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Human Lung ◽  
Smooth Muscle Actin ◽  
Lung Fibroblasts ◽  
Proteomic Profiling ◽  
Two Dimensional Gel Electrophoresis ◽  
Collagen Contraction ◽  
Extracellular Matrix Components ◽  
Fetal Fibroblasts ◽  
Adult Fibroblasts

Acute lung injury involving extremely immature lungs often heals without excessive fibrosis unlike later in gestation and in adults. Several factors may be involved, but fibroblast contraction of collagen has been linked to the level of wound fibrosis. To assess whether human lung fibroblasts of fetal versus adult origin differ in ability to contract collagen and define the molecular underpinnings, we performed three-dimensional collagen contraction assay, analyzed their differential mRNA profile, specifically for transforming growth factor-β (TGF-β) signaling pathway and extracellular matrix components, studied the cell response to TGF-β in culture, and used two-dimensional gel electrophoresis followed by mass spectrometry to identify differences in their overall proteomes. Human lung fetal fibroblasts contracted the collagen matrix less than the adults. Smooth muscle actin expression did not differ. TGF-β stimulation resulted in greater Smad3 phosphorylation in fetal compared with adults. mRNA and proteomic profiling reveal a number of TGF-β pathways, ECM components, and cytoskeletal regulatory molecules are differentially expressed between the cell types. Of note is TGF-β receptor interacting protein 1 (TRIP-1), which we show inhibits fibroblast collagen contraction and is higher in fetal than adult fibroblasts. We conclude that human lung fetal fibroblasts are less able to contract collagen than adult lung fibroblasts. The diminished ability is not due to impediment of Smad3 activation but rather, at least in part, due to their higher level of TRIP-1 expression. TRIP-1 is a novel modulator of fibroblast collagen contraction.

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