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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible contributions of the angiotensin receptor subtypes 1 (AT1) and 2 (AT2) to angiotensin II (Ang II)-induced changes in collagen secretion and production were studied using the specific angiotensin AT1- and AT2-receptor antagonists telmisartan and P-186, respectively. Cardiac fibroblasts (from normal male adult rats) from passage 2 were cultured to confluency and incubated in the presence of 10(-10) to 10(-6) M Ang II in serum-free Dulbecco's MEM medium for 24 hours. Collagen production and secretion were assayed by'H-Proline incorporation; non-collagen production and secretion were also calculated. Ang II dose-dependently increased collagen secretion and production in rat adult cardiac fibroblasts in culture. Non-collagen secretion and production were also concentration-dependently increased by Ang II. Addition of 100 nmol/l Ang II increased (p<0.01) collagen secretion and production bv 75+/-6 (SEM)% and 113+/-23%, respectively, and non-collagen secretion and production by 65+/-6% and 57+/-16%, respectively. Pretreatment of cardiac fibroblasts with telmisartan completely blocked the Ang II-induced increase in collagen secretion (p<0.001) and production(p<0.05) and in non-collagen secretion (p<0.01) and production (p<0.01). P-186 had no effect on the Ang II-induced increase in collagen secretion and production. Addition of telmisartan and P-186 did not affect collagen secretion and production in basal cardiac fibroblasts. Our data demonstrate that the effects of Ang II on collagen secretion and production in adult rat cardiac fibroblasts in culture are AT1-receptor mediated, since they were abolished by the specific AT1-receptor antagonist, telmisartan, but not by the specific AT2-receptor antagonist, P-186.
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PMID:Angiotensin II-induced stimulation of collagen secretion and production in cardiac fibroblasts is mediated via angiotensin II subtype 1 receptors. 1188 Nov 10

In order to generate a calcium-phosphate bone cement as a transient replacement for bone defects, we modified Biocement D (Merck Biomaterial GmbH) containing mineralised collagen with osteocalcin, the most abundant non-collageneous protein of bone. Osteocalcin was added to the cement paste during setting in order to control the crystallisation kinetics of hydroxyapatite (HAP) as well as to stimulate the interaction of osteoblasts and osteoclasts with the bone replacement material. Analysis by SEM and AFM shows, that the addition of osteocalcin causes a nanosize microstructure of the calcium cement, which can be explained by inhibited growth of HAP crystals. The fracture strength of the material decreased by incorporation of osteocalcin, pointing onto a higher defect concentration of the crystalline structure. The impact of osteocalcin onto the interaction of bone cells with HAP-Collagen I-cements was studied in a cell culture system using the human osteosarcoma cell line SAOS-2. Results suggest, that osteocalcin might possibly improve the initial adherence of osteoblast-like cells, whereas proliferation of the cells is not effected.
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PMID:Influence of osteocalcin and collagen I on the mechanical and biological properties of Biocement D. 1220 87

Type X collagen is principal extracellular matrix (ECM) in natural dermis. To prepare artificial dermis, collagen is traditional, and most superior biomaterial. But beside collagen, the dermis also contains many other ECM. Among them, glycosaminoglycan (GAG) is another important substance. To imitate the natural dermis, and modificate the scaffold materials, two types of scaffolds were prepared: one is traditional type X collagen spongy scaffold, the other is collagen-chondroitin sulfate (CS) spongy scaffold. Collagen was blended with CS, one kind of GAG, and cross-linked by 1-ethyl-3-(3-dimethyl aminopropyl) carbodiimide (EDC). Dermis fibroblast was isolated from neonate prepuce, and dermis fibroblasts were cultured on the scaffolds. The physical and chemical properties of the scaffolds were tested, including SEM, DSC, H&E staining, immunohistochemical staining and CS content analysis and so on. The results indicated that EDC is an effective and non-cytotoxic cross-link reagent, and attaching CS into collagen scaffold could improve the stability and histocompatibility of scaffold.
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PMID:The modification of scaffold material in building artificial dermis. 1222 50

Corneas of tadpole, mouse, rat, guinea pig, rabbit, cat, cattle, and human were examined by TEM and SEM in a comparative study. The differences between species were noted mainly by using TEM. Bowman's layer showed a tendency to be well developed in higher mammals. Tadpoles lack a Bowman's layer, lower mammals have a thin Bowman's layer, and higher mammals have a thick Bowman's layer. The boundary between the substantia propria and Descemet's membrane was distinct in higher mammals. On the other hand, there are no differences in thickness of the collagen fibrils that constitute Bowman's layer and those of the substantia propria. NaOH digestion was utilized for SEM preparation. SEM imaging revealed a textured appearance of the epithelial side of Bowman's layer. In Descemet's membrane, fibrous long spacing (FLS) fiber-like structures, which are arranged in parallel to the endothelium, were observed by both TEM and SEM. To our knowledge, this is the first report of SEM observations of FLS fiber-like structures on the endothelial surface of Descemet's membrane. SEM at a plane normal to the plane of the cornea showed that Descemet's membrane has a piled laminar structure. Descemet's membrane is closely associated with the collagen layer of the substantia propria. Collagen fibrils invading from the substantia propria into Descemet's membrane were observed with both TEM and SEM.
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PMID:Comparative observations on corneas, with special reference to Bowman's layer and Descemet's membrane in mammals and amphibians. 1238 95

The first indication of platelet activation is an increase in mean platelet volume (MPV). n-3 FA are known to inhibit platelet function and to reduce the risk for coronary heart disease. The purpose of this study was to determine the effects of EPA and DHA on MPV. Healthy subjects received olive oil placebo for 4 wk and then were randomly assigned to receive 4 g of ethyl esters of either safflower oil (n = 11), EPA (n = 10), or DHA (n = 12) for 4 wk. At the end of placebo run-in and treatment periods, MPV (fL; mean +/- SEM) and platelet count (PLT-CT; 10(3)/microL blood) were measured in the basal state and after ex vivo stimulation with collagen (10 microg/mL), cold (4 degrees C), and heat (37 degrees C). Unlike DHA, EPA lowered MPV as compared with safflower oil (7.2 +/- 0.1 vs. 7.5 +/- 0.1 fL; P < 0.05) and raised PLT-CT (211 +/- 18 vs.192 +/- 18 10(3)/microL; P < 0.05) in the fasting state. Collagen and cold significantly increased MPV whereas heat lowered MPV regardless of treatment. All stimuli decreased PLT-CT. EPA significantly increased platelet EPA (0.2 +/- 0.1 vs. 3.3 +/- 0.4%) and docosapentaenoic acid (DPA; 2.2 +/- 0.3 vs. 2.9 +/- 0.3%) concentrations, but not DHA. DHA treatment significantly increased DHA (1.4 +/- 0.2 vs. 4.1 +/- 0.5%) and DPA (2.0 +/- 0.4 vs. 3.0 +/- 0.4%) concentrations, but not EPA. In conclusion, EPA, but not DHA, reduces platelet activation, an early step in platelet aggregation.
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PMID:EPA, but not DHA, decreases mean platelet volume in normal subjects. 1253 May 52

The objective of this study was to observe and compare behavior of the collagen fiber microstructure in normal and healing ligaments, both in situ and ex vivo, in order to add insight into the structure-function relationship in normal and healing ligaments. Fifty-two ligaments from 26 male rats were investigated. Eleven animals underwent surgical transection of both medial collateral ligaments (MCLs) (22 ligaments), which were allowed to heal for a period of 2 weeks. An additional 15 animals (30 ligaments) were used as normals. Ligaments were placed into six groups: Slack (n = 6 control, n = 6 healing), Reference (n = 4 control, n = 4 healing), Loaded (n = 4 control, n = 4 healing), 15 degrees Flexion (n = 4 control, n = 4 healing), 120 degrees Flexion (n = 4 control, n = 4 healing), and Tissue Strain vs. Flexion Angle (n = 8 normals). All ligaments, except those in the Tissue Strain vs. Flexion Angle group, were prepared for scanning electron microscopy. Tissues were harvested, mounted in a load frame, and chemically fixed in one of five states: (1). slack, (2). reference (onset of loading), (3). loaded, (4). 15 degrees knee flexion, or (5). 120 degrees knee flexion. After fixation the tissues were prepared for electron microscopy (SEM). The micrographs from the slack, reference, and loaded groups show fiber straightening with loading in normal ligaments as well as in both scar and "retracted" regions of healing ligaments. Collagen fibers' diameter and crimp patterns were dramatically changed in the scar region of healing ligaments: Width decreased from 19.4 +/- 1.7 microm to 6.5 +/- 2.1 microm (p <.000001), period from 51.4 +/- 15.1 microm to 11.0 +/- 2.4 microm (p <.000001), and amplitude from 9.8 +/- 0.8 microm to 3.9 +/- 0.8 microm (p <.000001). Normal ligaments fixed in situ show wavy regions at 120 degrees but less so at 15 degrees flexion. Healing ligaments fixed in situ show regions of fiber waviness in the scar region at 120 degrees and also at 15 degrees flexion, indicating ligament laxity persists toward both extremes of the range of motion. The data suggest that straightening of crimped fibers is a functionally relevant phenomenon, not only in normal but also in healing ligaments.
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PMID:Scanning electron microscopic characterization of healing and normal rat ligament microstructure under slack and loaded conditions. 1274 72

This study evaluated the influence of collagen removal and the use of a low-viscosity liner on the marginal quality of composite restorations for the total-etch system, Prime & Bond 2.1 (PB) and the self-etching primer system, Clearfil SE Bond (CSEB), in high C-factor cavities with margins in dentin. High C-factor cavities were made on dentin exposed from ground labial surfaces of 100 bovine lower incisors, randomly assigned to 10 treatment groups and restored with composite Z 250, placed in bulk. In Group 1 (PB), control group, PB was applied according to the manufacturer's directions; in Group 2 (PB/PLF), an intermediate layer of low-viscosity composite Protect Liner F (PLF) was applied on the bonding resin surface; in Group 3 (PB/SH) following acid-etching, the surfaces were treated with 10% sodium hypochlorite (SH) for one minute and in Group 4 (PB/SH/PLF), the same procedure was conducted as for Group 3, plus an intermediate layer of PLF was applied as for Group 2. In Group 5 (CSEB), the control group, CSEB was applied according to the manufacturer's directions; in Group 6 (CSEB/PLF), an intermediate layer of PLF was applied; in Group 7 (SH/CSEB), the cavity surface was pre-treated with SH; in Group 8 (SH/CSEB/PLF), SH pre-treatment was conducted as for Group 7, then an intermediate layer of PLF was applied; in Group 9 (CSEB/SH), after CSEB-primer application, the surface was treated with SH, followed by CSEB-adhesive application and in Group 10 (CSEB/SH/PLF), the same was conducted as for Group 9, then an intermediate layer of PLF was applied. The specimens were stored at 37 degrees C for 24 hours, polished, molded and replicas were obtained in epoxy resin. The replicas were gold-sputter coated and observed by SEM (300x) for marginal quality classification. The Kruskal-Wallis non-parametrical multi-comparison Test (p<0.05) was used to obtain statistical analysis of the data. Results demonstrated that both adhesive systems in the control groups presented low marginal quality and a high variability. The use of an intermediate layer of PLF significantly improved the marginal quality with the CSEB system but had no effect with the PB system. Collagen depletion with SH enhanced marginal quality for the PB system and did not influence the CSEB system results.
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PMID:The effect of collagen removal and the use of a low-viscosity resin liner on marginal adaptation of resin composite restorations with margins in dentin. 1287 23

Collagen is often used in bioartificial livers as a biomimetic coating to promote liver cell adhesion and differentiation. Animal proteins are expensive and expose the host to risks of cross-species infection due to contamination with prions. Silk fibroin (SF) is a biocompatible protein produced by Bombyx mori silk worms and possibly an alternative to collagen. We prepared SF-collagen blend films with different SF content adherent to the bottom of standard tissue culture dishes, and characterized their surface morphology by SEM, their wettability and examined them for their capacity to support rat liver cell adhesion and metabolism. Cell metabolism was characterized by estimating the rate at which cells eliminated ammonia and synthesized urea for up to 48h of culture. SF-containing films were smooth, clear and more wettable than collagen. Cells readily adhered, formed junctions and small size aggregates on all films. As many cells adhered on SF as on collagen films. Cell adhesion to high collagen content blend films could not be reliably estimated because cells dwelt in the large cavities in the film. The effect of SF on cell metabolism differed with the investigated metabolic pathway. However, cells on SF-containing films eliminated ammonia and synthesized urea at rates generally comparable to, for urea synthesis at times higher than, that of cells on collagen. These results suggest that silk fibroin is a suitable substratum for liver cell attachment and culture, and a potential alternative to collagen as a biomimetic coating.
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PMID:Adhesion and function of rat liver cells adherent to silk fibroin/collagen blend films. 1498 85

Characterization of the extracellular matrix of the temporomandibular joint (TMJ) disc is crucial to advancing efforts in tissue engineering the disc. However, the current literature is incomplete and often contradictory in its attempts to describe the nature of the TMJ disc matrix. The aim of this study was to identify the variation of key matrix components along the three axes of the porcine disc using ELISAs to quantify these matrix components, immunohistochemistry to identify their regional distribution, and SEM to examine collagen fiber diameter and orientation. The overall GAG content of the TMJ disc (including the dermatan sulfate proteoglycans) was 5.3+/-1.2% of the dry weight. Chondroitin sulfate, which comprised 74% of this total GAG content, was 4.4, 8.2, and 164 times more abundant than dermatan sulfate proteoglycan, keratan sulfate, and hyaluronic acid, respectively. In general, these GAGs were most concentrated in the intermediate zone of the TMJ disc, appearing in dense clusters, and least concentrated in the posterior band. Additionally, chondroitin sulfate was more abundant medially than laterally. Collagen II was discovered in trace amounts, with higher relative amounts in the intermediate zone. Collagen fibers were observed to run primarily in a ring-like fashion around the periphery of the disc and anteroposteriorly through the intermediate zone, with a mean fiber diameter of 18+/-9 mum. Characterization studies of the TMJ disc, including prior biomechanical and cell studies along with the current study of the extracellular matrix, collectively reveal a distinct character of the intermediate zone of the disc compared to its anterior and posterior bands.
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PMID:Quantitative analysis and comparative regional investigation of the extracellular matrix of the porcine temporomandibular joint disc. 1574 1

Collagen-induced arthritis (CIA), an approved animal model for rheumatoid arthritis, is thought to be a T cell-dependent disease. There is evidence that CD8+ T cells are a major subset controlling the pathogenesis of CIA. They probably contribute to certain features of disease, namely tissue destruction and synovial hyperplasia. In this study we examined the role of perforin (pfp), a key molecule of the cytotoxic death pathway that is expressed mainly in CD8+ T cells, for the pathogenesis of CIA. We generated DBA/1J mice suffering from mutations of the pfp molecule, DBA/1J-pfp-/-, and studied their susceptibility to arthritis. As a result, pfp-deficient mice showed a reduced incidence (DBA/1J-pfp+/+, 64%; DBA/1J-pfp-/-, 54%), a slightly delayed onset (onset of disease: DBA/1J-pfp+/+, 53 +/- 3.6; DBA/1J-pfp-/-, 59 +/- 4.9 (mean +/- SEM), and milder form of the disease (maximum disease score: DBA/1J-pfp+/+, 7.3 +/- 1.1; DBA/1J-pfp-/-, 3.4 +/- 1.4 (mean +/- SEM); P < 0.05). Concomitantly, peripheral T cell proliferation in response to the specific antigen bovine collagen II was increased in pfp-/- mice compared with pfp+/+ mice, arguing for an impaired killing of autoreactive T cells caused by pfp deficiency. Thus, pfp-mediated cytotoxicity is involved in the initiation of tissue damage in arthritis, but pfp-independent cytotoxic death pathways might also contribute to CIA.
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PMID:Perforin deficiency attenuates collagen-induced arthritis. 1598 90


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