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At least 73 records · Page 4Linked to original sources
PubMed1977

Rheological studies of matrix--special reference on the mobility of leucocytes in relation to the rheological characters of experimental matrix.

The rheological characteristics of a model matrix, consisting of Bacto-agar, were correlated with the ability of the matrix to permit cellular penetration, using a rheolometer and the agar bullet method. The most important rheologic characteristic that affected cellular mobility was found to be the viscosity rate. A viscosity rate under 1,000 X 10(4) dyne sec/cm2 was needed to permit cellular mobility.

Adhesiveness↗
PubMed1986

Organization of the connective matrix of the sarcoid granuloma. Evolution and cell-matrix interactions.

The connective matrix of sarcoid granulomas is polymorphic. Immunolabeling techniques show that it is partly composed of fibronectin and collagen types I and III and is found at all stages of the granulomas' evolution. This suggests that the process known as hyalinization is not due to changes in the composition of the matrix but results from a gradual accumulation of connective tissue components. Fibronectin seems to play an essential role as mediator between different cell populations during the evolution of the granulomas.

Abdomen↗
PubMed1985

Platelet interaction with subendothelial extracellular matrix: platelet-fibrinogen interactions are essential for platelet aggregation but not for the matrix-induced release reaction.

Cultured endothelial cells produce an extracellular matrix (ECM) to which platelets adhere and spread, ultimately resulting in platelet aggregation, thromboxane B2 production, and serotonin release. We have investigated the role of fibrinogen binding to the platelet GPIIb/IIIa complex in these reactions by comparing normal platelet-rich plasma (PRP), PRP from patients with Glanzman's thrombasthenia (whose platelets lack the GPIIb/IIIa complex), PRP in the presence of a monoclonal antibody that blocks the binding of fibrinogen to the GPIIb/IIIa complex, platelets washed free of fibrinogen, and washed platelets to which fibrinogen was added. Although platelet aggregation was virtually completely inhibited in the samples in which the normal interaction between fibrinogen and GPIIb/IIIa was impaired, adhesion of platelets to the matrix, spreading, and release of [14C]-serotonin were not affected. All of the platelet preparations released significant amounts of T X B2 with time, but there was a decrease in the amount produced by both the thrombasthenic and antibody-treated platelets. We conclude that the interaction of fibrinogen with platelet GPIIb/IIIa is not required for platelet adhesion to ECM or for adhesion-induced shape change or serotonin release. On the other hand, the platelet-fibrinogen interaction may play some role in augmenting adhesion-induced T X B2 production, and it is absolutely required for adhesion-induced platelet aggregation.

Animals↗
PubMed1992

Interactions between HIV-infected monocytes and the extracellular matrix: increased capacity of HIV-infected monocytes to adhere to and spread on extracellular matrix associated with changes in extent of virus replication and cytopathic effects in infected cells.

Monocytes express cell surface receptors for extracellular matrix (ECM) proteins of basement membranes. These receptors are engaged during extravasation of cells through capillary endothelium into tissue. The number of human immunodeficiency virus (HIV)-infected monocytes that adhered to ECM over 2 h was threefold higher than that of uninfected control cells. This difference was ECM specific and was not observed with a bovine serum albumin substrate. Enhanced adhesion to ECM was evident in monocytes by 4 days after HIV infection and increased through 10 days. Monocytes exposed to a T cell-tropic HIV strain that binds to but does not replicate in monocytes showed no changes in adherence to ECM. Thus, productive infection of monocytes by HIV induces a significant increase in the capacity of these cells to interact with ECM. Enhanced adhesion of HIV-infected monocytes to ECM was associated with increased spreading: at 12 h, sixfold more HIV-infected monocytes were spread on ECM than were uninfected control cells. Cell processes of HIV-infected monocytes formed a complex network on ECM: many of these cells expressed HIV proteins as detected by indirect immunofluorescence. HIV-associated cytopathic effects and levels of virion-associated reverse transcriptase activity depended on the substrate to which monocytes were attached. Virus replication and cytopathic effects in monocytes adhered to ECM, fibronectin, or plastic alone were comparable. In contrast, HIV-infected monocytes attached to laminin showed a significant increase in virus replication and in extent of cytopathic effects through 2 weeks after infection. The lowest levels of HIV replication and cytopathic effects were in monocytes attached to collagen IV. Interactions between monocytes and ECM profoundly affect the manner in which these cells control HIV infection: HIV infection changes the capacity of infected monocytes to attach and spread on ECM; attachment to ECM alters the extent of virus replication in infected cells.

Cell Adhesion↗
PubMed1989

Structure of the gene for cartilage matrix protein, a modular protein of the extracellular matrix. Exon/intron organization, unusual splice sites, and relation to alpha chains of beta 2 integrins, von Willebrand factor, complement factors B and C2, and epidermal growth factor.

The entire gene for chicken cartilage matrix protein (CMP) has been isolated and characterized by restriction mapping, electron microscopy, nuclease S1 mapping, and sequence analysis. The gene, which is present in a single copy in the chicken genome, is 18 kilobase pairs long and comprises eight exons and seven introns. It has two transcription initiation sites, 8 base pairs from each other. A sequence very homologous to the consensus nuclear factor III binding-site sequence, a CAT- and a TATA-like sequence are found in the promoter region and ATTAAA is used as a polyadenylation signal. The nucleotide sequence defines a primary translation product of 493 amino acids which consists of a 23-amino acid signal peptide and two large repeated domains connected by an epidermal growth factor module. Amino acid sequences homologous to those of the repeated domains are present in the type A repeats of von Willebrand factor, complement factors B and C2, and in the alpha chains of the integrins Mac-1, p150,95, and LFA-1. The exon-intron structure indicates that the CMP gene may have arisen by exon duplication and exon shuffling during evolution. The GT-AG splice rule cannot be applied for the excision of the last intron of the CMP pre-mRNA. The donor splice site of intron G is basically different from the consensus sequence indicating that a novel type of splicing mechanism might exist in cartilage.

Amino Acid Sequence↗
PubMed1985

Immunological analysis of chick notochord and cartilage matrix development with antisera to cartilage matrix macromolecules.

Transverse frozen sections from the postcephalic region of stage 9-16 chick embryos and from the wing bud region of stage 17-31 embryos were stained with antibodies to the major extracellular matrix components of cartilage. These probes included unfractionated A1 and A2 antisera to the major cartilage proteoglycan, affinity-purified purified antibodies to the proteoglycan core protein and to Type II collagen, and a monoclonal antibody to keratan sulfate. In embryos as early as stage 10, notochord stained specifically with the keratan sulfate monoclonal antibody. At this stage the notochord, as well as surrounding tissues, were negative to cartilage proteoglycan and collagen antibodies. Positive staining with the latter probes was coordinately acquired by notochord cells and their accompanying sheath around stage 15, while surrounding tissues remained negative. At this stage, the ventral region of the perispinal cord sheath exhibited light staining with the proteoglycan and keratan sulfate antibodies though failing to react to Type II collagen antibodies. Positive staining of notochord and ventral spinal cord persisted through later developmental stages. As revealed by immunofluorescence, definitive vertebral chondroblasts first emerged at approximately stage 23 and definitive limb chondroblasts at stage 25. The results are discussed in terms of the possible multiple roles of notochord in early embryogenesis.

Animals↗
PubMed1989

Activation of matrix metalloproteinase 3 (stromelysin) and matrix metalloproteinase 2 ('gelatinase') by human neutrophil elastase and cathepsin G.

The ability of human neutrophil elastase and cathepsin G to activate matrix metalloproteinase 3 (MMP-3 = stromelysin) and MMP-2 ('gelatinase') purified from human rheumatoid synovial fibroblasts in culture was examined. The zymogen of MMP-3 (proMMP-3) was activated to full activity with elastase and cathepsin G by limited proteolysis of the molecule into two active forms of Mr approximately 45,000 and Mr approximately 25,000. In contrast, proMMP-2 was not activated at all by these neutrophil serine proteinases, although it was degraded into small fragments. These data suggest that neutrophil elastase and cathepsin G may play an important role in the activation of proMMP-3 in vivo in various inflammatory conditions, but proMMP-2 may be activated in different ways.

Cathepsin G↗
PubMed1988

Recognition of influenza A matrix protein by HLA-A2-restricted cytotoxic T lymphocytes. Use of analogues to orientate the matrix peptide in the HLA-A2 binding site.

CTL specific for the influenza A virus matrix peptide 57-68 and restricted by HLA-A2 were studied. Their ability to recognize a set of analogue peptides, each of which differed from the natural peptide by a single amino acid, was analyzed. This revealed a core of five amino acids, 61-65, where one or more changes completely abrogated recognition. The glycine at position 61 was the only residue where no substitution was tolerated. Analogue peptides that did not induce CTL-mediated lysis were tested as competitors with the natural peptide; those with substitutions at positions 60, 64, and 65 inhibited, identifying residues that interact with the TCR. Another approach was to test a set of four CTL clones on all of the analogues. Marked differences in recognition by individual CTL clones were observed for several substituted peptides. The data indicate that most of the analogues bind to HLA-A2 with possible differences in fine positioning of the peptide. An alpha helical orientation for the peptide is discussed.

Binding Sites↗
PubMed1991

Microvasculature in germinal matrix layer: its relationship to germinal matrix hemorrhage.

Microvasculature in the germinal matrix layer (GML) was studied by postmortem microangiography and stereomicroscopic observation on cleared specimens in methyl salicylate. A number of arterioles from penetrating and medullary branches of main cerebral arteries were distributed in the GML, forming a fine network of arterioles anastomosing with each other. Many venules in the GML converged at a few points and drained into subependymal veins. The main converging zone of venules was situated inside the GML close to the border zone of the GML and adjacent cerebral parenchyma. The converging zone coincided with the site of GML hemorrhage. Thus, many factors, including both venous and arterial, appear to influence circulation in the GML; ultimately the converging zones become overloaded and rupture, leading to GML hemorrhage.

Angiography↗
PubMed1989

Growth rate of human fibroblasts is repressed by the culture within reconstituted collagen matrix but not by the culture on the matrix.

Effect of reconstituted type I collagen gel on in vitro growth of fibroblasts was examined. A prolonged lag period was observed by culture either on the surface of three-dimensional collagen gel ("on-gel") or within the gels ("in-gel") as compared with the culture on plastic dishes. The rate of cell proliferation in logarithmic phase growth was repressed by the culture "in-gel" but not by the culture "on-gel". The differential growth rates between "in-gel" culture and "on-gel" culture should be ascribed to difference in distributions of interacting sites between cell and collagen fibrils. The repression of cell growth was more marked in a contracting collagen gel which contains higher density of collagen fibrils. The cell density in contracted gel per unit cross-section area was found to be much lower than that of confluent monolayer culture. These results suggest that the repression of cell growth by collagen fibrils in the three-dimensional gels is not due to direct cell-cell contact, but due to the distribution and number of contact sites between a cell and collagen fibrils.

Cell Count↗