Develoapmet of a Tissue Analog for Cartilage Repair

1991 ◽  
Vol 252 ◽  
Author(s):  
J. M. Pachence ◽  
S. R. Frenkel ◽  
H. Lin
Keyword(s):  
Type I Collagen ◽  
Collagen Matrix ◽  
In Vitro Studies ◽  
In Vivo Studies ◽  
Type I ◽  
Collagen Matrices ◽  
Pore Sizes ◽  
The Matrix

ABSTRACTPurified type I collagen was formed into matrices whose pore sizes were defined on the basis of previous results. The first series of in vitro studies measured the metabolism of chondrocytes grown in matrices with various pore sizes; results revealed that the growth rate was independent of the average matrix pore size, but that ckmdrocyte infiltration throughout the matrix was optimal for pore sizes of 100 to 150 un. In a second series of studies, type I collagen was combined with hyaluranic acid; the HyA/collagen matrices had little effect on chcrdrocyte cell growth versus the collagen matrices. A third set of in vitro studies used collagen matrices incorporating varying cornentrations of insulin-like growth factor. It was found that the IGF-1/collagen matrices can significantly effect the growth and metabolism of the clxrihrocytes. These experiments were vital in establishing the collagen matrix parameters which will be used in subsequent in vivo studies.

Cells in regenerating deer antler cartilage provide a microenvironment that supports osteoclast differentiation

2001 ◽  
Vol 204 (3) ◽  
pp. 443-455
Author(s):  
C. Faucheux ◽  
S. Nesbitt ◽  
M. Horton ◽  
J. Price
Keyword(s):  
Type I Collagen ◽  
Mononuclear Cells ◽  
Osteoclast Differentiation ◽  
Cathepsin K ◽  
Collagen Matrix ◽  
Tartrate Resistant Acid Phosphatase ◽  
Type I ◽  
Deer Antler

Deer antlers are a rare example of mammalian epimorphic regeneration. Each year, the antlers re-grow by a modified endochondral ossification process that involves extensive remodelling of cartilage by osteoclasts. This study identified regenerating antler cartilage as a site of osteoclastogenesis in vivo. An in vitro model was then developed to study antler osteoclast differentiation. Cultured as a high-density micromass, cells from non-mineralised cartilage supported the differentiation of large numbers of osteoclast-like multinucleated cells (MNCs) in the absence of factors normally required for osteoclastogenesis. After 48 h of culture, tartrate-resistant acid phosphatase (TRAP)-positive mononuclear cells (osteoclast precursors) were visible, and by day 14 a large number of TRAP-positive MNCs had formed (783+/−200 per well, mean +/− s.e.m., N=4). Reverse transcriptase/polymerase chain reaction (RT-PCR) showed that receptor activator of NF κ B ligand (RANKL) and macrophage colony stimulating factor (M-CSF) mRNAs were expressed in micromass cultures. Antler MNCs have the phenotype of osteoclasts from mammalian bone; they expressed TRAP, vitronectin and calcitonin receptors and, when cultured on dentine, formed F-actin rings and large resorption pits. When cultured on glass, antler MNCs appeared to digest the matrix of the micromass and endocytose type I collagen. Matrix metalloproteinase-9 (MMP-9) may play a role in the resorption of this non-mineralised matrix since it is highly expressed in 100 % of MNCs. In contrast, cathepsin K, another enzyme expressed in osteoclasts from bone, is only highly expressed in resorbing MNCs cultured on dentine. This study identifies the deer antler as a valuable model that can be used to study the differentiation and function of osteoclasts in adult regenerating mineralised tissues.

Cellular and humoral responses to collagen–polyvinylpyrrolidone administered during short and long periods in humans

2003 ◽  
Vol 81 (11) ◽  
pp. 1029-1035 ◽  
Author(s):  
Janette Furuzawa-Carballeda ◽  
Emilio Rojas ◽  
Mahara Valverde ◽  
Irma Castillo ◽  
Lino Diaz de León ◽  
...  
Keyword(s):  
Dna Damage ◽  
Type I Collagen ◽  
Cellular Damage ◽  
In Vivo Studies ◽  
Type I ◽  
Healthy Donors ◽  
Collagen Antibodies ◽  
Humoral Responses

Collagen, particularly type I, and its related derivatives have been extensively employed in many areas of pharmacology. The present study was performed to determine the safety of collagen–polyvinylpyrrolidone (collagen–PVP) by in vitro and in vivo studies. Sera and peripheral blood cells from healthy donors without treatment and patients treated with collagen–PVP were evaluated. We observed that the biodrug does not stimulate lymphoproliferation or DNA damage in vitro, nor does it induce human anti-porcine type I collagen or anti-collagen–PVP antibodies in vivo. Furthermore, no hepatic or renal metabolic dysfunctions were observed when collagen–PVP was administered by intradermal or intramuscular routes in short- or long-term treatments. In conclusion, the present work shows that no cellular damage or immunological adverse effects (cellular and humoral) occurred during collagen–PVP treatment, even after more than 400 weeks of consecutive administrations.Key words: collagen–polyvinylpyrrolidone, DNA damage, collagen antibodies, hypertrophic scar.

scholarly journals Complex Regional Pain Syndrome Type I, a Debilitating and Poorly Understood Syndrome. Possible Role for Pulsed Electromagnetic Fields: A Narrative Review

2017 ◽  
Vol 6 (20;6) ◽  
pp. E807-E822 ◽  
Author(s):  
Francesca Veronesi
Keyword(s):  
Inflammatory Cytokines ◽  
Pain Syndrome ◽  
In Vitro Studies ◽  
In Vivo Studies ◽  
Type I ◽  
Pulsed Electromagnetic Fields ◽  
Syndrome Type ◽  
Pulsed Electromagnetic

Background: Complex regional pain syndrome type I (CRPS-I), also called algodystrophy, is a complex syndrome characterized by limb pain, edema, allodynia, hyperalgesia and functional impairment of bone with a similar clinical picture of osteoporosis, including an increased release of various pro-inflammatory neuropeptides and cytokines. Several treatments have been proposed for CRPS-I, but due to the poor outcome of conventional drugs and the invasiveness of some techniques, expectations are now directed towards new resources that could be more effective and less invasive. Objective: In the light of preclinical evidence, which underlined pulsed electromagnetic fields’ (PEMFs) properties on osteoblasts (OBs), osteoclasts (OCs), and pathologies with an inflammatory profile, the present review aims to investigate whether there is a rationale for the use of PEMFs, as a combined approach, in CRPS-I. Study Design: This review analyzed the 44 in vitro and in vivo studies published in the last decade that focused on 2 main aspects of CRPS-I: local osteoporosis (OP) and inflammation. Setting: Not applicable. Methods: This review includes in vitro and in vivo studies found with a PubMed and Web of Knowledge database search by 2 independent authors. The limits of the search were the publication date between January 1, 2006, and January 1, 2016, and English language. In detail, the search strategy was based on: 1) CRPS-I or algodystrophy; 2) OP, OCs, and OBs; and 3) inflammatory aspects. Results: The included studies looked at the relationship between PEMFs and OCs (2 in vitro studies), osteoporotic animal models (8 in vivo studies), OBs (20 in vitro studies), inflammatory cytokines, and reactive oxygen species. They also tried to define the molecular cell pathways involved (5 in vivo and 9 in vitro studies on inflammatory models). It was observed that PEMFs increased OC apoptosis, OB viability, bone protein and matrix calcification, antioxidant protein, and the levels of adenosine receptors, while it decreased the levels of pro-inflammatory cytokines. Limitations: Data from clinical trials are scarce; moreover, experimental conditions and PEMF parameters are not standardized. Conclusions: The present review underlined the rationale for the use of PEMFs in the complex contest of CRPS-I syndrome, in combination with conventional drugs.

scholarly journals Control of Bone Matrix Properties by Osteocytes

2021 ◽  
Vol 11 ◽  
Author(s):  
Amy Creecy ◽  
John G. Damrath ◽  
Joseph M. Wallace
Keyword(s):  
Type I Collagen ◽  
Bone Matrix ◽  
Type I ◽  
Bone Homeostasis ◽  
Surrounding Matrix ◽  
Matrix Properties ◽  
The Matrix ◽  
Exciting Potential

Osteocytes make up 90–95% of the cellular content of bone and form a rich dendritic network with a vastly greater surface area than either osteoblasts or osteoclasts. Osteocytes are well positioned to play a role in bone homeostasis by interacting directly with the matrix; however, the ability for these cells to modify bone matrix remains incompletely understood. With techniques for examining the nano- and microstructure of bone matrix components including hydroxyapatite and type I collagen becoming more widespread, there is great potential to uncover novel roles for the osteocyte in maintaining bone quality. In this review, we begin with an overview of osteocyte biology and the lacunar–canalicular system. Next, we describe recent findings from in vitro models of osteocytes, focusing on the transitions in cellular phenotype as they mature. Finally, we describe historical and current research on matrix alteration by osteocytes in vivo, focusing on the exciting potential for osteocytes to directly form, degrade, and modify the mineral and collagen in their surrounding matrix.

scholarly journals The inhibitory effect of plasma fibronectin on collagen-induced platelet aggregation

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 450-457 ◽  
Author(s):  
DG Moon ◽  
JE Kaplan ◽  
JE Mazurkewicz
Keyword(s):  
Platelet Aggregation ◽  
Type I Collagen ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
In Vivo Model ◽  
Type I ◽  
Plasma Fibronectin ◽  
Antithrombotic Effect

Plasma fibronectin (Fn) has been proposed to have an antithrombotic effect, protecting against platelet and fibrinogen consumption after injury. The current study was designed to determine the effect of plasma fibronectin on collagen-induced platelet aggregation. In vitro aggregometry using an isolated homologous rat system, demonstrated a significant (P less than .05) inhibitory effect of 120 micrograms/mL Fn on platelet aggregation as induced by 60 micrograms/mL fibrillar collagen (type I). The inhibition was evidenced by a threefold increase in lag time and a significant decrease in the rate and extent of aggregation. The hypothesis was also tested using an in vivo model of collagen-induced platelet aggregation. The model used was intravenous injection of 2 mg/kg of homologous type I collagen into anesthetized Sprague-Dawley rats. Injection of collagen preincubated with 4 mg/kg Fn resulted in significantly less thrombocytopenia and fibrinogen consumption as compared with injection of collagen alone. The results of both the in vitro and in vivo studies are consistent with the proposed antithrombotic effect of plasma fibronectin.

scholarly journals The inhibitory effect of plasma fibronectin on collagen-induced platelet aggregation

Blood ◽  
1986 ◽  
Vol 67 (2) ◽  
pp. 450-457 ◽  
Author(s):  
DG Moon ◽  
JE Kaplan ◽  
JE Mazurkewicz
Keyword(s):  
Platelet Aggregation ◽  
Type I Collagen ◽  
Inhibitory Effect ◽  
In Vivo Studies ◽  
In Vivo Model ◽  
Type I ◽  
Plasma Fibronectin ◽  
Antithrombotic Effect

Abstract Plasma fibronectin (Fn) has been proposed to have an antithrombotic effect, protecting against platelet and fibrinogen consumption after injury. The current study was designed to determine the effect of plasma fibronectin on collagen-induced platelet aggregation. In vitro aggregometry using an isolated homologous rat system, demonstrated a significant (P less than .05) inhibitory effect of 120 micrograms/mL Fn on platelet aggregation as induced by 60 micrograms/mL fibrillar collagen (type I). The inhibition was evidenced by a threefold increase in lag time and a significant decrease in the rate and extent of aggregation. The hypothesis was also tested using an in vivo model of collagen-induced platelet aggregation. The model used was intravenous injection of 2 mg/kg of homologous type I collagen into anesthetized Sprague-Dawley rats. Injection of collagen preincubated with 4 mg/kg Fn resulted in significantly less thrombocytopenia and fibrinogen consumption as compared with injection of collagen alone. The results of both the in vitro and in vivo studies are consistent with the proposed antithrombotic effect of plasma fibronectin.

scholarly journals NMDA Receptor-mediated CaMKII/ERK Activation Contributes to Renal Fibrosis

2019 ◽  
Author(s):  
Jingyi Zhou ◽  
Shuaihui Liu ◽  
Luying Guo ◽  
Rending Wang ◽  
Jianghua Chen ◽  
...  
Keyword(s):  
Western Blot ◽  
Renal Fibrosis ◽  
Type I Collagen ◽  
Ischemia Reperfusion ◽  
In Vivo Studies ◽  
Type I ◽  
Erk Activation ◽  
Expression Levels

Abstract Background: Renal fibrosis (RF) results in renal function impairment and eventually kidney failure. We found that N-methyl-D-aspartate receptor (NMDAR) played an important role during RF. However, its mechanism of action is yet to be deciphered. Methods: RF was induced in vivo by unilateral ureteral obstruction (UUO) using 8-week-old C57BL/6 mice. The expression levels of the NMDAR’s functional subunit, NR1, was downregulated using lentiviral vector-mediated shRNA interference. Histological changes were observed using Masson’s trichrome staining. Expression of NR1, fibrotic markers (α-smooth muscle actin (α-SMA), type I collagen (COL1A4), S100A4 and fibronectin), and EMT markers (snail and E-cadherin) were measured using immunohistochemistry and western blot analysis. RF was induced after TGF-β-treatment in HK-2 cells in vitro. NMDAR antagonist MK-801 and Ca2+/calmodulin-dependent protein kinase II (CaMKII) antagonist KN-93 were included in this study for pathway determination. Expression of NR1, total and phosphorylation of CaMKII (p-CaMKII), total and p-ERK were measured using western blot and immunofluorescent assays. Results from in vitro studies were confirmed using in vivo studies for NR1, CaMKII and ERK expression levels. In addition, ischemia-reperfusion injury (IRI) mouse model was used to determine whether oral NMDAR inhibitor dextromethorphan (DXM) could inhibit chronic fibrosis. Results: Increased NR1 expression was observed in both UUO-injured kidneys and TGF-β-treated tubular cells. NR1 knockdown and MK801 administration downregulated CaMKII/ERK activation. In vitro administered CaMKII antagonist KN93 reduced ERK phosphorylation and was not affected by NR1 expression levels. DXM protected IRI-injured kidneys from atrophy and fibrosis. Conclusions: NMDAR participates in renal fibrogenesis by activating the CaMKII/ERK pathway. NMDAR could be a potential therapeutic target for renal fibrosis.

scholarly journals Regulation of Cell Invasion and Morphogenesis in a Three-Dimensional Type I Collagen Matrix by Membrane-Type Matrix Metalloproteinases 1, 2, and 3

2000 ◽  
Vol 149 (6) ◽  
pp. 1309-1323 ◽  
Author(s):  
Kevin Hotary ◽  
Edward Allen ◽  
Antonello Punturieri ◽  
Ikuo Yana ◽  
Stephen J. Weiss
Keyword(s):  
Type I Collagen ◽  
Proteolytic Enzymes ◽  
Mdck Cells ◽  
Three Dimensional ◽  
Collagen Matrix ◽  
Type I ◽  
Matrix Remodeling ◽  
The Matrix ◽  
Membrane Type

During tissue-invasive events, migrating cells penetrate type I collagen-rich interstitial tissues by mobilizing undefined proteolytic enzymes. To screen for members of the matrix metalloproteinase (MMP) family that mediate collagen-invasive activity, an in vitro model system was developed wherein MDCK cells were stably transfected to overexpress each of ten different MMPs that have been linked to matrix remodeling states. MDCK cells were then stimulated with scatter factor/hepatocyte growth factor (SF/HGF) to initiate invasion and tubulogenesis atop either type I collagen or interstitial stroma to determine the ability of MMPs to accelerate, modify, or disrupt morphogenic responses. Neither secreted collagenases (MMP-1 and MMP-13), gelatinases (gelatinase A or B), stromelysins (MMP-3 and MMP-11), or matrilysin (MMP-7) affected SF/HGF-induced responses. By contrast, the membrane-anchored metalloproteinases, membrane-type 1 MMP, membrane-type 2 MMP, and membrane-type 3 MMP (MT1-, MT2-, and MT3-MMP) each modified the morphogenic program. Of the three MT-MMPs tested, only MT1-MMP and MT2-MMP were able to directly confer invasion-incompetent cells with the ability to penetrate type I collagen matrices. MT-MMP–dependent invasion proceeded independently of proMMP-2 activation, but required the enzymes to be membrane-anchored to the cell surface. These findings demonstrate that MT-MMP–expressing cells can penetrate and remodel type I collagen-rich tissues by using membrane-anchored metalloproteinases as pericellular collagenases.

Transplantation of Adipose-derived Cells for Periodontal Regeneration: A Systematic Review

2019 ◽  
Vol 14 (6) ◽  
pp. 504-518 ◽  
Author(s):  
Dilcele Silva Moreira Dziedzic ◽  
Bassam Felipe Mogharbel ◽  
Priscila Elias Ferreira ◽  
Ana Carolina Irioda ◽  
Katherine Athayde Teixeira de Carvalho
Keyword(s):  
Systematic Review ◽  
Animal Models ◽  
Platelet Rich Plasma ◽  
Periodontal Regeneration ◽  
In Vitro Studies ◽  
In Vivo Studies ◽  
Cell Sources ◽  
Study Designs

This systematic review evaluated the transplantation of cells derived from adipose tissue for applications in dentistry. SCOPUS, PUBMED and LILACS databases were searched for in vitro studies and pre-clinical animal model studies using the keywords “ADIPOSE”, “CELLS”, and “PERIODONTAL”, with the Boolean operator “AND”. A total of 160 titles and abstracts were identified, and 29 publications met the inclusion criteria, 14 in vitro and 15 in vivo studies. In vitro studies demonstrated that adipose- derived cells stimulate neovascularization, have osteogenic and odontogenic potential; besides adhesion, proliferation and differentiation on probable cell carriers. Preclinical studies described improvement of bone and periodontal healing with the association of adipose-derived cells and the carrier materials tested: Platelet Rich Plasma, Fibrin, Collagen and Synthetic polymer. There is evidence from the current in vitro and in vivo data indicating that adipose-derived cells may contribute to bone and periodontal regeneration. The small quantity of studies and the large variation on study designs, from animal models, cell sources and defect morphology, did not favor a meta-analysis. Additional studies need to be conducted to investigate the regeneration variability and the mechanisms of cell participation in the processes. An overview of animal models, cell sources, and scaffolds, as well as new perspectives are provided for future bone and periodontal regeneration study designs.

scholarly journals Effects of chitosan-collagen dressing on wound healing in vitro and in vivo assays

2021 ◽  
Vol 19 ◽  
pp. 228080002198969
Author(s):  
Min-Xia Zhang ◽  
Wan-Yi Zhao ◽  
Qing-Qing Fang ◽  
Xiao-Feng Wang ◽  
Chun-Ye Chen ◽  
...  
Keyword(s):  
Wound Healing ◽  
Wound Dressing ◽  
Type I Collagen ◽  
Inhibition Zone ◽  
Negative Control ◽  
Type I ◽  
Nih3t3 Cells ◽  
Post Operation

The present study was designed to fabricate a new chitosan-collagen sponge (CCS) for potential wound dressing applications. CCS was fabricated by a 3.0% chitosan mixture with a 1.0% type I collagen (7:3(w/w)) through freeze-drying. Then the dressing was prepared to evaluate its properties through a series of tests. The new-made dressing demonstrated its safety toward NIH3T3 cells. Furthermore, the CCS showed the significant surround inhibition zone than empty controls inoculated by E. coli and S. aureus. Moreover, the moisture rates of CCS were increased more rapidly than the collagen and blank sponge groups. The results revealed that the CCS had the characteristics of nontoxicity, biocompatibility, good antibacterial activity, and water retention. We used a full-thickness excisional wound healing model to evaluate the in vivo efficacy of the new dressing. The results showed remarkable healing at 14th day post-operation compared with injuries treated with collagen only as a negative control in addition to chitosan only. Our results suggest that the chitosan-collagen wound dressing were identified as a new promising candidate for further wound application.

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