scholarly journals Permeable type I collagen membrane promotes glomerular epithelial cell growth in culture

1993 ◽  
Vol 43 (2) ◽  
pp. 470-478 ◽  
Author(s):  
Kazuo Nosaka ◽  
Tadahiro Nishi ◽  
Hiromi Imaki ◽  
Keiji Suzuki ◽  
Shoji Kuwata ◽  
...  
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Type I Collagen ◽  
Collagen Membrane ◽  
Type I ◽  
Glomerular Epithelial Cell

scholarly journals Combining Sandblasting, Alkaline Etching, and Collagen Immobilization to Promote Cell Growth on Biomedical Titanium Implants

Polymers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 2550
Author(s):  
Chia-Fei Liu ◽  
Kai-Chun Chang ◽  
Ying-Sui Sun ◽  
Diem Thuy Nguyen ◽  
Her-Hsiung Huang
Keyword(s):  
Cell Growth ◽  
Type I Collagen ◽  
Bone Cells ◽  
Surface Characteristics ◽  
Attenuated Total Reflection ◽  
Titanium Implants ◽  
Type I ◽  
Alkaline Etching ◽  
Marrow Mesenchymal Stem Cells ◽  
Collagen Immobilization

Our objective in this study was to promote the growth of bone cells on biomedical titanium (Ti) implant surfaces via surface modification involving sandblasting, alkaline etching, and type I collagen immobilization using the natural cross-linker genipin. The resulting surface was characterized in terms topography, roughness, wettability, and functional groups, respectively using field emission scanning electron microscopy, 3D profilometry, and attenuated total reflection-Fourier transform infrared spectroscopy. We then evaluated the adhesion, proliferation, initial differentiation, and mineralization of human bone marrow mesenchymal stem cells (hMSCs). Results show that sandblasting treatment greatly enhanced surface roughness to promote cell adhesion and proliferation and that the immobilization of type I collagen using genipin enhanced initial cell differentiation as well as mineralization in the extracellular matrix of hMSCs. Interestingly, the nano/submicro-scale pore network and/or hydrophilic features on sandblasted rough Ti surfaces were insufficient to promote cell growth. However, the combination of all proposed surface treatments produced ideal surface characteristics suited to Ti implant applications.

scholarly journals Role of collagenase in mediating in vitro alveolar epithelial wound repair

1999 ◽  
Vol 112 (2) ◽  
pp. 243-252
Author(s):  
E. Planus ◽  
S. Galiacy ◽  
M. Matthay ◽  
V. Laurent ◽  
J. Gavrilovic ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Type I Collagen ◽  
Alveolar Epithelial Cell ◽  
Cell Monolayer ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial

Type II pneumocytes are essential for repair of the injured alveolar epithelium. The effect of two MMP collagenases, MMP-1 and MMP-13 on alveolar epithelial repair was studied in vitro. The A549 alveolar epithelial cell line and primary rat alveolar epithelial cell cultures were used. Cell adhesion and cell migration were measured with and without exogenous MMP-1. Wound healing of a cell monolayer of rat alveolar epithelial cell after a mechanical injury was evaluated by time lapse video analysis. Cell adhesion on type I collagen, as well as cytoskeleton stiffness, was decreased in the presence of exogenous collagenases. A similar decrease was observed when cell adhesion was tested on collagen that was first incubated with MMP-1 (versus control on intact collagen). Cell migration on type I collagen was promoted by collagenases. Wound healing of an alveolar epithelial cell monolayer was enhanced in the presence of exogenous collagenases. Our results suggest that collagenases could modulate the repair process by decreasing cell adhesion and cell stiffness, and by increasing cell migration on type I collagen. Collagen degradation could modify cell adhesion sites and collagen degradation peptides could induce alveolar type II pneumocyte migration. New insights regarding alveolar epithelial cell migration are particularly relevant to investigate early events during alveolar epithelial repair following lung injury.

scholarly journals Treatment with type-I collagen scaffolds in patients with venous ulcers. Case report

Case reports ◽  
2020 ◽  
Vol 6 (2) ◽  
pp. 128-136
Author(s):  
Martha Isabel González-Duque ◽  
Julián Daniel Hernández-Martínez ◽  
Marta Raquel Fontanilla ◽  
Sofía Elizabeth Muñoz-Medina
Keyword(s):  
Type I Collagen ◽  
Low Cost ◽  
Adult Population ◽  
Lower Limbs ◽  
Collagen Membrane ◽  
Type I ◽  
Dermal Substitute ◽  
Collagen Scaffolds ◽  
Venous Ulcers

Introduction: Chronic venous insufficiency affects about 5% of the global adult population. Venous leg ulcers are one of the most frequent complications of this pathology, with a global prevalence of 2%. This disease affects both the quality of life of patients and, due to the high cost of the treatment, the health system. Compressive therapy and moist wound healing have been the gold standard treatment. However, when complications occur, they may not be effective.Case report: This is the case of a 66-year-old female patient with venous ulcers on her lower limbs and symptoms of fever and local pain that did not respond to conventional therapies. The patient was treated with a new dermal substitute made of an acellular type-I collagen membrane, which promotes the closure of the ulcer by stimulating the replacement of injured tissue with tissue similar to the healthy one. The condition of the patient improved at 16 weeks, and after 8 months of treatment there was no recurrence of the lesions.Conclusions: Acellular type-I collagen membrane developed by the Tissue Engineering Working Group of the Department of Pharmacy of the Universidad Nacional de Colombia is effective in treating venous ulcers of the lower limbs. Its low cost facilitates the access of the whole population to therapies based on its application.

Extracellular matrix regulates proliferation and phospholipid turnover in glomerular epithelial cells

1990 ◽  
Vol 259 (2) ◽  
pp. F326-F337 ◽  
Author(s):  
A. V. Cybulsky ◽  
J. V. Bonventre ◽  
R. J. Quigg ◽  
L. S. Wolfe ◽  
D. J. Salant
Keyword(s):  
Extracellular Matrix ◽  
Growth Factors ◽  
Dna Synthesis ◽  
Type I Collagen ◽  
Collagen Matrix ◽  
High Dose ◽  
Type I ◽  
Glomerular Injury ◽  
Glomerular Epithelial Cell ◽  
Phospholipid Turnover

To understand how glomerular epithelial cell (GEC) growth might be regulated in health and disease, we studied the effects of growth factors and extracellular matrix on proliferation and membrane phospholipid turnover in cultured rat GECs. In GECs adherent to type I collagen matrix, epidermal growth factor (EGF), insulin, and serum stimulated DNA synthesis and increased cell number. In addition, GECs proliferated when adherent to type IV collagen, but not to laminin or plastic substrata. Attachment of GECs to the substrata that facilitated proliferation (types I or IV collagen) produced increases in 1,2-diacylglycerol (DAG), an activator of protein kinase C (PKC). Increased DAG was associated with hydrolysis of inositol phospholipids and an increase in inositol trisphosphate and was not dependent on the presence of growth factors. After PKC downregulation (by preincubation with a high dose of phorbol myristate acetate), DNA synthesis was enhanced in GECs adherent to collagen. Thus contact of GECs with collagen matrices is required for serum, EGF, or insulin to induce proliferation. Collagen matrix also activates phospholipase C. As a result, the DAG-PKC signaling pathway desensitizes GECs to the mitogenic effects of growth factors and might promote cell differentiation. Understanding the interaction between GECs, growth factors, and extracellular matrix may elucidate the mechanisms of proliferation during glomerular injury.

scholarly journals Histamine Induces ATP Release from Human Subcutaneous Fibroblasts, via Pannexin-1 Hemichannels, Leading to Ca2+ Mobilization and Cell Proliferation

2013 ◽  
Vol 288 (38) ◽  
pp. 27571-27583 ◽  
Author(s):  
Ana Rita Pinheiro ◽  
Diogo Paramos-de-Carvalho ◽  
Mariana Certal ◽  
Maria Adelina Costa ◽  
Cristina Costa ◽  
...  
Keyword(s):  
Cell Growth ◽  
Pyridoxal Phosphate ◽  
Type I Collagen ◽  
Prolonged Exposure ◽  
Atp Release ◽  
Receptor Activation ◽  
Disulfonic Acid ◽  
Type I ◽  
Reactive Blue 2 ◽  
Pannexin 1

Changes in the regulation of connective tissue ATP-mediated mechano-transduction and remodeling may be an important link to the pathogenesis of chronic pain. It has been demonstrated that mast cell-derived histamine plays an important role in painful fibrotic diseases. Here we analyzed the involvement of ATP in the response of human subcutaneous fibroblasts to histamine. Acute histamine application caused a rise in intracellular Ca2+ ([Ca2+]i) and ATP release from human subcutaneous fibroblasts via H1 receptor activation. Histamine-induced [Ca2+]i rise was partially attenuated by apyrase, an enzyme that inactivates extracellular ATP, and by blocking P2 purinoceptors with pyridoxal phosphate-6-azo(benzene-2,4-disulfonic acid) tetrasodium salt and reactive blue 2. [Ca2+]i accumulation caused by histamine was also reduced upon blocking pannexin-1 hemichannels with 10Panx, probenecid, or carbenoxolone but not when connexin hemichannels were inhibited with mefloquine or 2-octanol. Brefeldin A, an inhibitor of vesicular exocytosis, also did not block histamine-induced [Ca2+]i mobilization. Prolonged exposure of human subcutaneous fibroblast cultures to histamine favored cell growth and type I collagen synthesis via the activation of H1 receptor. This effect was mimicked by ATP and its metabolite, ADP, whereas the selective P2Y1 receptor antagonist, MRS2179, partially attenuated histamine-induced cell growth and type I collagen production. Expression of pannexin-1 and ADP-sensitive P2Y1 receptor on human subcutaneous fibroblasts was confirmed by immunofluorescence confocal microscopy and Western blot analysis. In conclusion, histamine induces ATP release from human subcutaneous fibroblasts, via pannexin-1 hemichannels, leading to [Ca2+]i mobilization and cell growth through the cooperation of H1 and P2 (probably P2Y1) receptors.

Integrin mediation of alveolar epithelial cell migration on fibronectin and type I collagen

1997 ◽  
Vol 273 (1) ◽  
pp. L134-L141 ◽  
Author(s):  
H. J. Kim ◽  
C. A. Henke ◽  
S. K. Savik ◽  
D. H. Ingbar
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Type I Collagen ◽  
Alveolar Epithelial Cell ◽  
Matrix Proteins ◽  
Type I ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Beta 1 Integrin ◽  
Alpha V Beta 3

Acute lung injury leads to type I alveolar epithelial cell (AEC) death, denudation of the alveolar basement membrane, and formation of an alveolar provisional matrix from fibronectin, fibrinogen, and type I collagen. The provisional matrix provides a scaffold for alveolar repair. To restore normal lung architecture, surviving type II AECs must reepithelialize denuded alveoli. We examined whether AECs migrate on provisional matrix proteins and whether integrins mediate this migration using a Boyden chemotaxis chamber. Cultured AECs migrated on fibronectin-coated filters by haptotaxis (defined as movement on a solid-phase substrate) more than one type I collagen-coated filters, and they did not migrate on fibrinogen-coated filters. Soluble fibronectin augmented migration on type I collagen-coated filters, but not on fibronectin-coated filters. Anti-alpha v beta 3-integrin monoclonal antibody (MAb) inhibited migration on substrate-bound fibronectin by 62-77%, whereas anti-beta 1-integrin MAb inhibited migration by 48%. Anti-alpha 2-integrin MAb almost completely inhibited migration on substrate-bound type I collagen, but not on fibronectin. The novel findings in this study are as follows: 1) AECs migrate by haptotaxis more effectively on substrate-bound fibronectin than on type I collagen; 2) alpha v beta 3- and beta 1-integrins partially mediate AEC haptotaxis on fibronectin; and 3) the alpha 2 beta 1-integrin mediates AEC migration on type I collagen. These results support the importance of type II cell migration on provisional matrix proteins during repair of lung injury.

Sign in / Sign up

Export Citation Format

Share Document