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Biomedical subjects

S Gay

Publications and source records attributed to S Gay.

At least 271 records · Page 15Linked to original sources

Demonstration by immunofluorescence that the same cells from chick embryo aortas synthesize elastin and collagen types I and III.

Cells were isolated from the aortas of 17-day old chick embryos and they were stained with fluorescent antibodies specific for Type I collagen, Type I procollagen, Type III collagen, elastin and prolyl hydroxylase. The results indicated that the same cells simultaneously synthesize Type I procollagen, Type III procollagen and elastin. The synthesis of procollagens, and the presence of prolyl hydroxylase, in the same cells which synthesize elastin may well explain why elastin contains hydroxy-proline.

Animals↗

Inhibition of collagen-induced platelet aggregation by antibodies to distinct types of collagens.

Aggregation of platelets by fibrils formed from collagens type I, II and III could be inhibited by coating the fibrils with anti-collagen antibodies or Fab fragments. Similar results were obtained in a clot-retraction assay. Inhibition was achieved with stoichiometric amounts of antibodies and was specific for each type of collagen. Aggregation caused by a mixture of type-I and -III collagens could only be inhibited by a mixture of antibodies against both collagens. The data show that each interstitial collagen is capable of interacting with platelets and do not support the concept of an outstanding activity of type-III collagen.

Antibodies↗

Immunohistochemical demonstration of basement membrane collagen in normal human skin and in psoriasis.

Antibodies prepared against the collagen C-chain derived from human placenta specifically strain the epidermal basement membrane of normal human skin as well as the basement membrane surrounding the skin appendages and capillaries. Using the antibodies, it was observed that all basement membranes in untreated psoriatic plaques appear fragmented and separted into several layers. The results suggest that psoriatic lesions are associated with a general loss of basement membrane integrity which may play a crucial role in the pathogenesis of the disease.

Antibody Specificity↗

Changes in the surface of the mouse blastocyst at implantation.

Implantation is a critical event, and perhaps the earliest one, in the maternal recognition of pregnancy. Information transfer from conceptus to mother might occur during, and subsequent to, implantation at the level of cell surface interaction. Therefore, attempts have been made both to identify the phases of implantation during which changes in the blastocyst surface occur and to characterized such changes. In vitro, blastocysts have been found to go through a series of discrete steps which are analogous to implantation in utero, and these steps can be retarded or prevented by the use of either suboptimal culture media or an inappropriate substratum. Morphological surface changes are not apparent when the blastocyst becomes adherent to the substratum; however, marked differences in blastocyst surface structure are revealed by scanning electron microscopy at the onset of trophoblast outgrowth. Studies at the molecular level implicate collagen as having a role in blastocyst adhesiveness, but other cell surface components are also likely to be involved.

Animals↗

Collagen in the cellular and fibrotic stages of scleroderma.

The collagen in localized and systemic scleroderma skin was studied by light microscopy with silver impregnation (50 patients), electron microscopy (14 patients), and immunofluorescence microscopy using specific antibodies against Type I and Type III collagens (12 patients). In the cellular stage, the dermis and adipose tissue revealed perivascular or diffuse cellular infiltrates (mostly lymphocytes, plasma cells, and macrophages), accompanied by deposition of Type III collagen. The lower dermis also showed an increase in Type III collagen. In the fibrotic stage, the papillary layer showed a reduction and/or clumping of Type III collagen as compared to normal skin. The lower dermis and the adipose tissue revealed compact collagen consisting exclusively of Type I collagen or a mixture of Type I and Type III collagen. The pattern of Type III collagen distribution was similar to that of reticulin, thus suggesting that at least some reticulin fibrils may represent Type III collagen.

Adipose Tissue↗

Scleroderma.

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Adult↗

Collagen types in early phases of wound healing in children.

Small silicone rubber tubes containing a standard size viscose cellulose sponge (Cellstic) were implanted in wounds of ten children at the end of surgery. The Cellstics were drawn out of the wound 24--120 hours after implantation and the cellulose sponges were sectioned and studied for collagen types. Immunologically detectable Type III collagen and procollagen was detected in the sponges 24--48 hours after implantation whereas Type I collagen was not found at that time. From hour 72 onwards a substantial increase in Type I collagen was noted, while the relatively low levels of Type I procollagen remained unchanged. The levels of Type III collagen and procollagen increased only slightly. Primary cultures from 9-day-old granulation tissue synthesized preferentially Type I collagen, on the basis of chromatographic analysis. We conclude that Type III collagen is produced at the earliest phases of wound healing by primitive mesenchymal cells followed by the production of Type I collagen after the appearance of mature wound fibroblasts.

Adolescent↗

Dermal architecture and collagen type distribution.

The human dermis consists of two morphologically different layers. A loose meshwork of thin collagenous fibres is characteristic for the adventitial dermis with includes the papillary and the periadnexal dermis. Thick, coarse collagen bundles are the main feature of the reticular dermis. Two different collagens, type I and type III occur in the dermis as shown previously by biochemical analyses. Antibodies specific for type I collagen or type III collagen and their corresponding precursors were used in indirect immunofluorescence tests to localize the various collagens in frozen sections of normal adult skin. Whereas type I collagen is found in all dermal layers, the main part of type III collagen can be found within the adventitial dermis. Antibodies against the precursor of type I collagen stain only a bandlike region immediately beneath the epidermis. Antibodies against the precursor of type III collagen stain the same regions as antibodies against the helical part of type III collagen.

Antibodies↗

Presence of type III collagen in bone from a patient with osteogenesis imperfecta.

Samples of bone from a patient with osteogenesis imperfecta were found to synthesize and contain type III collagen as well as type I collagen. Normal bone contains only type I collagen except in the lining cells of the bone marrow cavities. In the patient's tissue, type III collagen was localized in nonfibrillar structures in discrete areas of the bone. These and previous studies indicate that certain types of osteogenesis imperfecta may be caused by a failure of normal bone maturation and the sites in which the type III collagen is found appear to be defects in the bone.

Bone Development↗

Immunhistochemical demonstration of different collagen types in the normal epiphyseal plate and in benign and malignant tumors of bone and cartilage.

Several benign and malignant tumors of bone and cartilage were examined by means of type-specific collagen antibodies in connection with indirect immunofluorescence technique in order to determine wether there is a positive correlation between cell morphology and gene expression as refered to the synthesis of tissue- or cell-specific collagen. In general benign bone and cartilage tumors show the collagen type corresponding to the original maternal tissue. In malignant osteogenic tumors a strong positive correlation was found between morphologic differentiation of osteosarcoma cells and tissue specific collagen synthesarcomas. Unrelated to the grade of differentiation and the type of malignant tumor, collagen type III could be demonstrated in all tumors investigated, occurring rather from vascular stroma than from the tumor cell itself.

Bone Neoplasms↗

Transitions in collagen types during matrix-induced cartilage, bone, and bone marrow formation.

The localization of types I, II, and III collagens during bone matrix-induced sequential differentiation of cartilage, bone, and bone marrow was studied by specific immunofluorescence. Subcutaneous transplantation of coarse powders of demineralized rat bone matrix into allogeneic recipients resulted in new bone formation. After a transient appearance of polymorphonuclear leukocytes in the implant, fibroblasts appeared in close continguity to the matrix on day 3. Type III collagen was then localized as a fine network around the invading fibroblasts. On days 4--6 smaller amounts of type I were also detected around these proliferating cells. With the onset of chondrogenesis, type II collagen was detected in the cartilage matrix on day 6 and persisted until the early stages of bone formation. Vascular invasion of the implant was accompanied by osteogenesis on day 10. Type I collagen was demonstrated in the newly deposited bone matrix coating the surfaces of cartilage spicules and particles of implanted bone powder. On day 17 and thereafter, type III collagen was localized as a fibrous array around nests of hematopoietic cells.

Animals↗