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Biomedical subjects

G Gabbiani

Publications and source records attributed to G Gabbiani.

At least 271 records · Page 15Linked to original sources
PubMed1975

Malignant soft tissue tumors of probable histiocytic origin (malignant fibrous histiocytomas): general considerations and electron microscopic and tissue culture studies.

Correlated light and electron microscopic study of four fibrous histiocytomas of proven malignancy has confirmed the presence of histiocyte-like and fibroblast-like cells in this tumor. In addition, an undifferentiated cell type, giant cells, xanthomatous cells, and rare cells with morphological characteristics intermediate between those of histiocytes and fibroblasts were seen. "Nuclear body" type inclusions were commonly present in both principal cell types in all four cases, as were the somewhat less common cytoplasmic inclusion bodies. Electron microscopic study of a tissue culture of one of these tumors demonstrated only fibroblast-like, histiocyte-like, and xanthomatous cells. The possibility is suggested that both principal cell types in this tumor may derive from the same undifferentiated stem cell.

Adult↗
PubMed1975

Actin in the cytoplasm of adrenocortical cells.

Rat or hamster adrenocortical cells contain a network of filaments mostly 40-80 A in diameter, which is particularly evident at the cell periphery. In frozen sections, adrenocortical cells fix (particularly at their periphery) anti-actin autoantibodies present in sera of patients with chronic aggressive hepatitis. It is concluded that the peripheral network of adrenocortical cells contains contractile proteins (at least actin) and the implication of such proteins in steroid secretion is discussed.

Actins↗
PubMed1975

Experimental focal glomerular lesions elicited by insoluble immune complexes. Ultrastructural and immunofluorescent studies.

Injection of small amounts of ferritin intravenously, into the aorta (above the renal arteries) or into the left renal artery of rabbits hyperimmunized against this protein, results in the formation of circulating, insoluble, antigen-antibody complexes. Some of these complexes localize focally in the renal glomerular capillaries, where they elicit severe lesions. The fate of the complexes and the evolution of the lesions have been followed by immunofluorescent and electron microscopic techniques. Within a few hours, the deposition of complexes in the glomeruli resulted in a massive accumulation of neutrophils platelets, and fibrin, sometimes leading to acute focal necroses of some loops. These lesions were quite similar to those developing in the small dermal vessels during the Arthus reaction. Most of the complexes were rapidly phagocytosed and degraded by neutrophils; swelling and proliferation of endothelial and mesangial cells usually followed the acute damage and contributed to the removal of remaining complexes, cell debris, and fibrin deposits. Later, focal areas of mesangial proliferation and sclerosis were observed, containing large amounts of basement membrane-like material and sometimes of collagen fibrils; synechiae and crescent formation were noted in certain places. These observations suggest that the glomerular localization of very large, poorly soluble or insoluble immune complexes may be responsible for the focal glomerular changes seen in association with subacute bacterial endocarditis, with anaphylactoid purpura, or for some of the most severe lesions developing during chronic immune complex diseases.

Animals↗
PubMed1975

Cytoplasmic contractile apparatus in aortic endothelial cells of hypertensive rats.

Hypertension was produced in male Wistar rats (150 gm. body weight) by complete ligature of the aorta between the renal arteries. Electron microscopic examination revealed that 1 week later the amount of cytoplasmic microfilaments in the endothelial cells of the aortic segment above the coarctation (mean blood pressure 160 mm. Hg) was strikingly increased as compared with normal animals. The endothelial cells in the segment below the coarctation (mean blood pressure 25 mm. Hg) contained few filaments and were similar to the cells in the aortic endothelium in controls (mean blood pressure 105 mm. Hg). Microfilaments measured 40 to 70 angstrom in diameter and were mostly located close to the endothelial clefts, where they formed longitudinal bundles or a network. The bundles of microfilaments contained electron-dense areas similar to the "attachment sites" of the underlying smooth muscle. By using en face preparations of aortic endothelial cells treated with antiactin autoantibodies (AAA) followed by anti-human IgG, it was seen that in hypertensive animals the cells above the ligature were intensely fluorescent when compared with those of the aortic portion below the ligature or those of the controls. The fluorescence was abolished after incubation of the AAA sera with thrombosthenin A. The correlation between electron microscopic and immunologic findings suggests that the microfilaments present in the endothelial cells of hypertensive animals are composed, at least in part, of actin. Endothelial cells so modified may play a role in permeability or may be related to other phenomena such as electrotonic coupling and synchronized contraction of aortic cells during hypertension.

Actins↗
PubMed1975

Contractile apparatus in aortic endothelium of hypertensive rat.

One week after hypertension was produced in male Wistar rats (150 g body weight) by a complete aortic ligature placed between renal arteries, electron microscopic studies showed a striking increase of cytoplasmic microfilaments in the endothelial cells of the aortic segment above coarctation (mean blood pressure 160 mm Hg). These microfilaments measured 40-70 A in diameter and were located particularly close to the endothelial clefts. In "en face" preparation of aortic endothelial cells treated with antiactin autoantibodies (AAA) followed by antihuman IgG, the cells above the ligature of hypertensive animals were intensely fluorescent compared with those of the aortic portion below the ligature or that of controls. The fluorescence was abolished after incubating the AAA-containing sera with thrombosthenin-A, suggesting the presence of actin. There was also an increase transport of horseradish peroxidase and ferritin through the endothelial cell layer. While endothelial cells so modified may play a role in permeability regulation, they may also be related to such mechanisms as electronic coupling and synchronized contraction of aortic cells during hypertension.

Actins↗
PubMed1974

"Contractile interstitial cells" in pulmonary alveolar septa: a possible regulator of ventilation-perfusion ratio? Ultrastructural, immunofluorescence, and in vitro studies.

In the lungs of healthy rats, humans, lambs, and monkeys, about 50% of the alveolar interstitial cells-resembling fibroblasts-contain bundles of fibrils measuring 30-80 A in diameter. Immunofluorescence studies on frozen sections of rat lung demonstrate that many interstitial cells bind sera containing antiactin antibodies. On account of these two sets of findings and our additional in vitro studies suggesting alveolar tissue contraction due to hypoxia or epinephrine, we postulate that the alveolar septa contain contractile cells different from that of smooth muscle. For these cells we propose the name of "contractile interstitial cells." Such cells lie within the thick portion of the air-blood barrier and around the pre- or postcapillary vessels. Hence it is possible that they play a role in the autoregulation of ventilation/perfusion (V/Q) ratio, particularly in hypoxic pulmonary hypertension. These findings, demonstrating a contractile system other than bronchial and arterial smooth muscle, suggest that the alveolus should no more be conceived as a passive "organ."

Animals↗
PubMed1973

Human smooth muscle autoantibody. Its identification as antiactin antibody and a study of its binding to "nonmuscular" cells.

When human serum containing smooth muscle autoantibodies (SMA) is incubated with extracts containing thrombosthenin (the contractile material of platelets) or thrombosthenin-A (the actin-like moiety of thrombosthenin), it loses its ability to bind to smooth muscle. Such binding is also diminished when SMA serum is incubated with lysed platelets; this effect is not seen if the SMA serum is incubated with intact platelets. The incubation of other autoantibodies (such as antimitochondrial or antinuclear antibodies) with thrombosthenin does not affect their binding to the specific antigens. It appears that SMA is directed against the actin fraction of thrombosthenin-ie, SMA is an antiactin antibody. Hence the name of antiactin autoantibody (AAA) seems more appropriate than smooth muscle autoantibody (SMA). A study of the distribution of antiactin autoantibody binding in rat, rabbit and man shows that several "nonmuscular" structures contain actin under normal conditions; these include megakaryocytes and platelets, normal rat hepatocytes, the brush borders of renal tubules, the periphery of epithelial cells of the intestine, polymorphs and lymphocytes in lymph nodes (but not thymic cortical lymphocytes). In addition, certain cell types (such as granulation tissue fibroblasts, cultivated fibroblasts, hepatocytes or regenerating liver and epidermal cells growing over a skin wound) can reversibly acquire a massive network of actin-containing microfilaments resembling those in smooth muscle.

Absorption↗