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Biomedical subjects

R Ross

Publications and source records attributed to R Ross.

At least 415 records · Page 23Linked to original sources
PubMed1975

Partial characterization of the shift from IgG to IgA synthesis in the clonal differentiation of human leukemic bone marrow-derived lymphocytes.

An unusual B-cell proliferation was noted in an individual (Tun) which was characterized by the presence of two separate populations of chronic lymphocytic leukemia (CLL) cell staining on the surface and in the cytoplasm for either IgG(k) or IgA(k). Utilizing an idiotypic antiserum prepared from the associated serum monoclonal IgG(k) protein the idiotype was detected on the surface and in the cytoplasm of both the IgG- and IgA-bearing cell populations. These observations are consistent with a common clonal origin and a switch mechanism involving IgG and IgA synthesis. Sequential-labeling of Surface Ig and intracellular Ig with antisera conjugated to opposite fluorochromes documented the progressive maturation of the terminal differentiation of the IgA-bearing cell population at a level before morphologically distinct plasma cells. The distribution and pattern of surface and cytoplasmic IgG and IgA staining in individual cells suggest that the direction of switching is from IgG to IgA synthesis. The demonstration of shared idiotypic specificity between the IgG- and IgA-bearing populations is consistent with a transition in Ig heavy chain synthesis resulting from an alternation in the CH gene. It is concluded that certain CLL clones may manifest a switch from IgG to IgA synthesis at a level of B-cell differentiation which encompasses both the B lymphocyte and the Ig-synthesizing plasma cell.

Animals↗
PubMed1975

Connective tissue cells, cell proliferation and synthesis of extracellular matrix-a review.

The ubiquitous connective tissues contain a wide range of cells including fibroblasts, osteoblasts and chondroblasts. Recently it has been demonstrated that another principal cell of the connective tissue is the smooth muscle cell in several organ systems. These have been shown to be responsible for the synthesis of the connective tissue matrix components of the uterine myometrium and of the arterial system, including collagen, both elastic fibre proteins and glycosaminoglycan. Microtubule inhibitors such as colchicine and vinblastine, and iron chelators such as alpha,alpha -dipyridyl have been used to study their morphologic and chemical effects on collagen synthesis and secretion. Colchicine produces an increase in large Golgi-associated vacuoles, which sometimes contain material reminiscent of aggregates of collagen macromolecules. Vinblastine produces alterations in the endoplasmic reticulum cisternae similar to alterations seen in ascorbic acid deficiency, and alpha,alpha-dipyridyl increases the frequency of regions in cells, interpretable as potential sites of communication of rough endoplasmic reticulum cisternae with the cell surface. Ferritin conjugated anti-procallagen sera were used to localize procollagen in cells and demonstrated procollagen not only in the cisternae of rough endoplasmic reticulum but in all of the elements of the Golgi complex as well. The studies reported in this review have shown that in cell culture arterial smooth muscle will produce not only the microfibrillar protein of the elastic fibre but soluble and/or insoluble elastin as well. Recent studies on serum factors responsible for the proliferation of connective tissue cells have demonstrated that at least one of the principal factors responsible for fibroblast and/or smooth muscle cell proliferation in culture is derived from thrombocytes. Medium containing serum derived from cell-free plasma lacks most of this proliferative effect which can be reinstated when platelets are present during recalcification to form serum. This effect is due to the platelet release reaction as shown by combining supernatant factors derived from platelets exposed to purified thrombin to cell-free, plasma derived serum. Studies with macrophages have also suggested that phagocytic macrophages release factor(s) into a cell culture medium that may also participate in stimulating fibroblasts to proliferate in vitro. The means by which these factors stimulate fibroblast proliferation and connective tissue synthesis remains to be elucidated.

Animals↗
PubMed1975

A radioautographic study of collagen synthesis by earthworm epidermis.

Secreation by the epidermis of two oligochaetes (Eisenia and Enchytraeus) was investigated radioautographically following administration of 3H-proline, 3H-tryptophan or Na2(35)SO4. Regionally epidermal columnar cells of Enchytraeus synthesize the overlying, probably collagenous, cuticle. Eisenia epidermis does not recordably synthesize the cuticle until after wounding (first eight segments removed). By two days postoperative the epidermal columnar cells of Eisenia synthesize the collagenous cuticle and, later in regeneration, the epidermis may simultaneously synthesize the different collagen of the underlying basement lamella. The epidermis of Enchytraeus, but not of Eisenia, synthesizes some sulfated material associated with the cuticle surface.

Animals↗
PubMed1975

Location of procollagen in chick corneal and tendon fibroblasts with ferritin-conjugated antibodies.

Three distinct antiprocollagen preparations were characterized and used in immunocytochemical staining of chick embryo corneal and tendon cells. The several ferritin-conjugated antibody preparations permitted similar location of procollagen in the cisternae of the rough endoplasmic reticulum and in Golgi elements in both cell types. The ability to demonstrate and interpret specific ferritin staining was dependent on the extent of membrane breakage in each of those organelles, coupled with adequate retention of cell morphology. Corneal fibroblasts appeared to suffer more extensive intracellular membrane damage under controlled conditions of homogenization than tendon fibroblasts, facilitating the identification of procollagen in Golgi vacuoles of these cells. None of the labeled material appeared to by cytoplasmic in origin since ferritin was observed in the cytoplasm only in the vicinity of Golgi elements that were extensively broken. This study extends previous immunological evidence for the presence of procollagen in the Golgi complex and calls attention to the problems to be encountered in locating the antigen in small Golgi vesicles and lamellae.

Animals↗
PubMed1975

Proteoglycans in primate arteries. I. Ultrastructural localization and distribution in the intima.

Proteoglycans were identified and localized histochemically and ultrastructurally in normal and hyperplastic arterial intimas in nonhuman primates (Macaca nemestrina). These regions were consistently more alcianophilic than the adjacent medial layers and this alcianophilia was absent after treatment with glycosaminoglycan-degradative enzymes. Ultrastructurally, the intimal intercellular matrix consisted of numerous, irregularly shaped, 200-500-A diameter granules possessing 30--60-A diameter filamentous projections, and these granules were dispersed between collagen and elastic fibers. The granules exhibited a marked affinity for ruthenium red and were interconnected via their filamentous projections. The ruthenium red-positive granules were intimately associated with the plasma membrane of intimal smooth muscle cells and attached to collagen fibrils and elastic fibers. The matrix granules were completely removed after testicular hyaluronidase or chondroitinase ABC digestion but only partially removed after leech hyaluronidase treatment. These results suggest that the matrix granules contain some hyaluronic acid and one or more isomers of chondroitin sulfate. In addition to the large ruthenium red-positive matrix granules, a smaller class of ruthenium red-positive granule (100--200-A diameter) was present within the basement membranes beneath the endothelium and surrounding the smooth muscle cells. Ruthenium red also exhibited an affinity for the surface coat of the smooth muscle cells. The potential importance of proteoglycans in arterial intimal hyperplasia is discussed.

Animals↗
PubMed1975

Proteoglycans in primate arteries. II. Synthesis and secretion of glycosaminoglycans by arterial smooth muscle cells in culture.

Glycosaminoglycan synthesis and secretion by primate arterial smooth muscle have been examined in cell culture. Mass cultures of diploid primate arterial smooth muscle cells were either double labeled with [35S]sulfate and [3H]acetate or single labeled with [3H]glucosamine for 24 h and glycosaminoglycans were extracted and isolated from the culture medium. Incorporation of labeled precursors into glycosaminoglycan was maximal during stationary phase of smooth muscle cell growth in culture and reduced, but not eliminated during logarithmic growth. The glycosaminoglycans synthesized and secreted into the culture medium were characterized by differential susceptibility to glycosaminoglycan-degradative enzymes and by cellulose acetate electrophoresis. Both assay procedures indicate that cultured primate arterial smooth muscle cells synthesize principally dermatan sulfate (60%-80% of total), chondroitin sulfate A and/or C (10%-20%of total) and little or no hyaluronic acid (0%-5% of total). This pattern of glycosaminoglycan formation differed significantly from that exhibited by isologous skin fibroblasts cultured under identical conditions. Dermal fibroblasts synthesize and secrete primarily hyaluronic acid (50%-60% of total) with lesser amounts of dermatan sulfate (10%-20% of total) and chondroitin sulfate A and/or C (10%-20% of total). These results indicate that differences exist in proteoglycan metabolism between these two connective tissue-producing cells in vitro, and suggest that the observed pattern of in vitro glycosaminoglycan synthesis by primate arterial smooth muscle cells may be characteristic for this cell type and not a general response to conditions of cell culture.

Animals↗
PubMed1975

Effect of insulin on the proliferation of cultured primate arterial smooth muscle cells.

Smooth muscle cells were grown from thoracic aortas of 1-year-old monkeys (Macaca nemistrina). The effect of insulin on the proliferation of these cells was studied by comparing the growth of cells in culture medium to which insulin had been added with that of cells in basal (1% monkey serum) medium and in growth-promoting 5% monkey serum. Insulin in concentrations of 10, 100, 1,000, and 10,000 muunits/ml resulted in successively greater stimulation of growth which was highly significant (P smaller than 0.001) by analysis of variance. There was a significant linear relationship between the logarithm of the insulin dose and cell growth. However, the highest concentration of insulin produced only 50% of the effect of 5% monkey serum. Serum from which insulin had been removed stimulated growth less well (P smaller than 0.05) than did untreated serum at the same concentration (5%) but had significant (P smaller than 0.05) stimulating properties compared with whole serum at a lower concentration. Cells that were older in culture life (eight or nine passages) did not show a growth response to insulin and had an attenuated response to 5% serum. The effect of insulin (100 muunits/ml) was inhibited by dibutyryl cyclic adenosine monophosphate (db-cAMP) (5 times 10-5 M), although there was a latent period of 3 days before inhibition occurred; db-cAMP had no effect on cell counts in the absence of insulin. The electron microscopic appearance of the cells was unaltered by insulin.

Analysis of Variance↗
PubMed1975

The role of the macrophage in wound repair. A study with hydrocortisone and antimacrophage serum.

The role of the monocyte/macrophage in wound repair has been investigated by studying the healing process in wounds depleted of this cell and/or its phagocytic activity. Hydrocortisone acetate (0.6 mg/g body weight) administered as a subcutaneous depot was used to induce a prolonged monocytopenia in guinea pigs, and antimacrophage serum (AMS) was used for local elimination of tissue macrophages. In vitro, the presence of complement, macrophages are rapidly lysed and used killed by AMS. In the absence of complement, AMS is not cytotoxic but potently inhibits adherence to and phagocytosis of opsonized erythrocytes by macrophages. AMS titers were obtained by observation of adherence and phagocytosis of opsonized erythrocytes in serial dilutions of AMS. Six groups of animals were studied: a) untreated animals, b)animals receiving daily subcutaneous injections of normal rabbit serum (NRS) around each wound, c)animals receiving daily subcutaneous AMS around each wound, d)animals receiving systemic hydrocortisone, e)animals receiving systemic hydrocortisone and daily injections of NRS around each wound, and f)animals receiving systemic hydrocortisone and daily AMS around each wound. Wounds consisted of a series of six linear incisions in the dorsal skin. Subcutaneous AMS alone has no effect on the number of circulating monocytes, nor was there any observable effect on the number or the phagocytic ability of wound macrophages. Fibrosis in these wounds was unaffected. Systemic hydrocortisone induced a prolonged monocytopenia. The macrophage level in the wounds of these monocytopenic animals was reduced to approximately one-third that of controls; the phagocytic activity of the monocytes/macrophages that did appear in these wounds was, however, similar to that of controls. Some inhibition of wound debridement was observed in these wounds, but fibrosis was virtually unaffected. Collagen synthesis, as judged morphometrically, was similar to that of control wounds at all stages of repair. Conjoint systemic hydrocortisone and subcutaneous AMS around each wound resulted in the almost complete disappearance of macrophages from the wounds. Wound fibrin levels were elevated, and clearance of fibrin, neutrophils, erythrocytes and other miscellaneous debris from these wounds was delayed. Fibroblasts, which in control wounds first appear by 3 days postwounding and reach maximal levels by day 5, did not appear in these wounds until day 5, and their subsequent rate of proliferation was slower than that of controls. Continued.

Animals↗
PubMed1974

A platelet-dependent serum factor that stimulates the proliferation of arterial smooth muscle cells in vitro.

Dialyzed serum from clotted monkey blood ("blood serum") promotes the proliferation of monkey arterial smooth muscle cells in culture, but dialyzed serum prepared from recalcified platelet-poor plasma ("plasma serum") is much less effective. Addition of platelets and calcium to platelet-poor plasma increases the activity of plasma serum to the same level achieved with blood serum. Furthermore, addition to plasma serum of a platelet-free supernatant prepared by exposing purified platelets to thrombin also stimulates the proliferation of smooth muscle cells. Thus, much of the growth-promoting activity of dialyzed serum is directly or indirectly derived from platelets. This finding has important implications for the response of arteries to localized injury and provides a key to further understanding of the role of factors derived from blood serum in promoting cell proliferation in vitro.

Animals↗
PubMed1974

Effects of antimicrotubular agents on the secretion of collagen. A biochemical and morphological study.

Embryonic chick cranial bone was cultured in the presence of the antimicrotubular agents, colchicine and vinblastine, and with a number of other compounds known from previous studies to affect the cellular handling of collagen. Secretion of procollagen, quantitated by light microscope autoradiography, was correlated with the extent of conversion of procollagen to collagen and with rates of collagen and noncollagen-protein synthesis. Colchicine inhibited procollagen secretion and conversion to collagen and specifically inhibited collagen synthesis. Cells exposed to colchicine revealed an increased number of dilated Golgi-associated vacuoles and vesicles, some of which contained parallel aggregates of filamentous structures. These observations suggest that the pathway of at least a fraction of procollagen secretion by osteoblasts includes the Golgi complex. Disruption of microtubules may interfere with the movement of Golgi-derived vesicles, and the resulting accumulation of collagen precursors in the Golgi complex may lead secondarily to an inhibition of synthesis. Although vinblastine also inhibited both procollagen secretion and conversion to collagen, the observed reduction in general protein synthesis and striking changes in the ultrastructure of the rough endoplasmic reticulum complicated interpretation of the effects. Interpretation of the effects of cytochalasin B was limited by the finding that the cellular response in cranial bone was markedly heterogeneous and that, contrary to some previous reports, the drug caused an inhibition in the incorporation of radiolabeled amino acids into both collagen and noncollagen protein.

Animals↗