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Biomedical subjects

H Senoo

Publications and source records attributed to H Senoo.

12 recordsLinked to original sources
PubMed1992

Simultaneous expression of type I procollagen mRNA and albumin in cirrhotic human liver.

The gene expression of human type I procollagen was investigated in cirrhotic human liver by using in situ hybridization with nonradioactive DNA probes. Using in situ hybridization can provide direct evidence for the cell type capable for type I collagen synthesis in tissues. T-T dimerized DNA probes were used and DNAs hybridized in situ were detected immunohistochemically using specific antibodies against T-T dimer. The data demonstrated that type I collagen is synthesized in hepatocytes and stellate cells in pseudolobules and in fibroblasts in Glissons capsules in cirrhotic human livers. We indicated hepatocytes morphologically and functionally by using immunohistochemical localization of albumin, which was used as a marker of hepatocyte, since albumin is synthesized exclusively by hepatocytes.

Adult↗
PubMed1990

Internalization of retinol-binding protein in parenchymal and stellate cells of rat liver.

We have studied uptake of retinol-binding protein (RBP) by rat liver cells. First, we compared the in vivo uptake in different liver cells of 125I-labeled RBP with that of other well-known ligands. We found that the ligands studied were recognized differently by the various cell types in the liver, and that RBP was most efficiently taken up by parenchymal and stellate cells. We then studied the in vivo uptake of RBP in liver cells by immunocytochemistry at the electron microscopic level using ultrathin cryosections. Ten min after injection, RBP was localized to parenchymal cells and stellate cells. In these cells, RBP was detected on the cell surface and in vesicles near the cell surface. RBP was observed mainly in association with the membrane in these vesicles. Two hours after injection, RBP was localized not only on the cell surface and in vesicles close to the cell surface, but also in larger vesicles located deeper in the cytoplasm of these cells. RBP in larger vesicles was observed at a distance from the vesicular membrane. Finally, we compared the distribution of endocytosed RBP in liver parenchymal cells with that of asialo-orosomucoid, a ligand known to be internalized by receptor-mediated endocytosis. We detected both ligands on the cell surface and in small vesicles located close to the cell surface and in larger vesicles located deeper in the cytoplasm. Asialo-orosomucoid and RBP were seldom observed in the same small vesicles, but the larger vesicles contained both ligands. These data suggest that RBP is internalized in parenchymal and stellate cells of the liver by receptor-mediated endocytosis.

Animals↗
PubMed1989

L-ascorbic acid 2-phosphate stimulates collagen accumulation, cell proliferation, and formation of a three-dimensional tissuelike substance by skin fibroblasts.

Proliferation of human skin fibroblasts was stimulated significantly by the presence of L-ascorbic acid 2-phosphate (Asc 2-P). The presence of Asc 2-P (0.1-1.0 mM) in the culture medium for 3 weeks enhanced the relative rate of collagen synthesis to total protein synthesis 2-fold as well as cell growth 4-fold. Coexistence of L-azetidine 2-carboxylic acid (AzC), an inhibitor of collagen synthesis, attenuated both effects of Asc 2-P in a dose-dependent manner. Supplementation of the medium with Asc 2-P also accelerated procollagen processing to collagen and deposition of collagen in the cell layer. Among the acidic glycosaminoglycans (GAG), another major component of extracellular matrix (ECM), deposition of sulfated forms was increased by the additive. Electron microscopic observations showed multilayered, rough endoplasmic reticulum-rich cells surrounded by dense ECM. These results indicate that Asc 2-P is useful in culture systems as a long-acting vitamin C derivative and also that it promotes reorganization of a three-dimensional tissuelike substance from skin fibroblasts in culture by stimulating collagen accumulation in the fibroblasts.

Ascorbic Acid↗
PubMed1989

Co-culture of fibroblasts and hepatic parenchymal cells induces metabolic changes and formation of a three-dimensional structure.

Co-culturing of tendon fibroblasts and liver parenchymal cells in Williams' medium E supplemented with fetal bovine serum, hormones, and L-ascorbic acid 2-phosphate, a long acting vitamin C derivative, resulted in formation of three-dimensional structure. Both growth of fibroblasts and their production of collagen were inhibited, however production of albumin by the hepatocytes was much better preserved than when individual cells were cultured separately, indicating epithelial-mesenchymal interactions stimulate reorganization of the liver-like tissue from isolated cells.

Achilles Tendon↗
PubMed1988

Regulation of collagen metabolism and cell growth by epidermal growth factor and ascorbate in cultured human skin fibroblasts.

Epidermal growth factor (2-50 ng/ml), prepared from mouse submaxillary glands, stimulated growth and the synthesis of non-collagenous proteins and hyaluronic acid, but inhibited collagen synthesis in cultured human skin fibroblasts, both stimulation and inhibition being dose-dependent. All these effects may be intrinsic functions of the epidermal growth factor molecule, because these effects were cancelled by the co-presence of antiserum specific for epidermal growth factor and because they were also observed following the addition of human epidermal growth factor produced urogastrone cDNA. On the other hand, L-ascorbate (vitamin C) stimulated growth and collagen synthesis, as well as synthesis of non-collagenous proteins, with no significant effect on hyaluronic acid synthesis. Co-presence of epidermal growth factor and ascorbate gave additive effects on growth and protein synthesis of the cells. These results suggest that the two growth-promoting factors, epidermal growth factor and L-ascorbate, modulate metabolism of extracellular matrix components as well as cell growth in a quite different manner in human skin fibroblasts.

Adult↗
PubMed1986

Two stages of the differentiation of HL-60 cells induced by 1 alpha,25 dihydroxyvitamin D3; commitment by 1 alpha,25 dihydroxyvitamin D3 and promotion by DMSO.

The differentiation of HL-60 cells induced by 1 alpha,25 dihydroxyvitamin D3 was found to be separated into two stages, i.e. commitment and promotion. Most of the HL-60 cells were committed to monocyte/macrophage lineage by pretreatment with 1 alpha,25 dihydroxyvitamin D3 (5-50 ng/ml) for 18-24 hr. The promotion in the second stage was inducer and lineage independent; treatment with 1.25% DMSO for 2 or 3 days promoted the differentiation of the committed HL-60 cells by 1 alpha,25 dihydroxyvitamin D3 into monocyte/macrophage lineage, but not granulocyte lineage.

Antibodies, Monoclonal↗
PubMed1986

Improved Kupffer's gold chloride method for demonstrating the stellate cells storing retinol (vitamin A) in the liver and extrahepatic organs of vertebrates.

This paper describes our modification of the classical gold chloride technique for the demonstration of the perisinusoidal stellate cells in the liver. The results of the method as introduced by von Kupffer (1876) are unpredictable. Using our modification, high quality gold preparations can be obtained. The method allows selective staining of retinol (vitamin A)-storing stellate cells in the liver and extrahepatic organs of various vertebrates. The sensitivity of the reaction is comparable to that of the fluorescence method for retinol. The technique is simple and the preparations keep for several years. Formol fixed specimens can be counterstained with Sudan III or hematoxylin. We have also developed a simple technique for making "sinusoid-net preparations," removing the parenchymal cells by supersonication. The clear visualization of the stellate cells that results has made it possible to study the distribution of these cells.

Animals↗
PubMed1985

Suppression of experimental hepatic fibrosis by administration of vitamin A.

The effect of vitamin A on experimental hepatic fibrosis in rats induced by administration of carbon tetrachloride (CCl4) and pig serum was studied. Vitamin A content in the CCl4-induced cirrhotic liver decreased significantly. Administration of pig serum caused hepatic fibrosis without hepatocytic damage. Vitamin A suppressed induction of experimental hepatic fibrosis by CCl4 and pig serum. Neither hepatocytic injury nor increased activities of serum aspartate aminotransferase and glutamic pyruvic transaminase induced by CCl4 was diminished by vitamin A. These data provide evidence that vitamin A inhibits hepatic fibrogenesis and that this effect may be mediated by an action on stellate cells rather than hepatocytes.

Animals↗