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Biomedical subjects

R Matsuda

Publications and source records attributed to R Matsuda.

At least 55 records · Page 3Linked to original sources

Platelet-derived growth factor in combination with collagen promotes the migration of human skin fibroblasts into a denuded area of a cell monolayer.

Since we have found previously that adult donor skin fibroblasts (TIG-114) migrated more slowly in serum-depleted medium than in medium supplemented with 10% FBS, we tried to identify a factor(s) which promotes fibroblast migration from the edge of a denuded area in a monolayer. In medium supplemented with 10% FBS, the effects of both suramin, a competitor of growth factors at the receptor level, and monensin, an inhibitor of the secretion of extracellular matrix, were examined. Both substances suppressed cell migration, suggesting that growth factors and matrix substances are important for cell migration. Then, we examined the effects of growth factors and extracellular matrix on fibroblast migration in serum-free medium. Platelet-derived growth factor (PDGF), basic fibroblast growth factor, acidic fibroblast growth factor, and transforming growth factor-beta did not stimulate cell migration. Type I collagen, plasma fibronectin, and heparin also did not promote cell migration. However, the combination of PDGF and type I collagen did promote cell migration. Addition of anti-PDGF antibody reduced the stimulatory effect induced by the combination of PDGF and type I collagen. These results suggest that the copresence of growth factors and extracellular matrix regulates fibroblast migration into a denuded area in a monolayer.

Adult↗

cis-4-Hydroxy-L-proline and ethyl-3,4-dihydroxybenzoate prevent myogenesis of C2C12 muscle cells and block MyoD1 and myogenin expression.

cis-4-Hydroxy-L-proline (cis-OH-Pro) and ethyl-3,4-dihydroxybenzoate (EDHB), two distinct inhibitors of collagen synthesis, prevented myogenesis in C2C12 mouse skeletal muscle cells. Both inhibitors blocked myotube formation and the expression of sarcomeric myosin heavy chain. Northern blot analysis showed that cis-OH-Pro- and EDHB-treated C2C12 muscle cells did not express the myogenic regulatory genes, MyoD1 and myogenin, but continued to express non-muscle isoforms of actin (beta and gamma) and alpha-tropomyosin. 10TFL2-3B cells, a C3H10T1/2 cell line permanently transfected with myogenin cDNA, constitutively expressed exogenous myogenin in the presence of cis-OH-Pro but failed to activate endogenous myogenin and to undergo myogenesis. These results demonstrate that commitment to terminal differentiation and activation of myogenic regulatory genes requires active synthesis of the extracellular matrix component collagen.

Animals↗

[Effects of Kamikihi-To on autonomic imbalances in SART-stressed (repeated cold-stressed) mice].

The effects of Kamikihi-To (KMK), a traditional Chinese medicine, on autonomic imbalances were evaluated in SART-stressed (repeated cold-stressed) mice. These animals exhibited decreases in pain threshold and contraction of duodenum by acetylcholine, and they showed changes in their electrocardiogram and hematological parameters. All symptoms are thought to be caused by dysautonomia. KMK in dosages of 0.5 and 1.0 g/kg were administered to mice once a day for 8 consecutive days. SART stress was induced from the second day. KMK prevented the decrease in the pain threshold and contraction of the duodenum, although it had no effect on the electrocardiographic or hematological changes. KMK had no similar effect on unstressed mice. This data suggests that KMK might be useful for the treatment of clinical autonomic imbalances.

Acetylcholine↗

[Suppressive effect of sialic acid on the prostaglandin E2-mediated edema in carrageenin-induced inflammation of rat hind paws].

We performed these studies to determine whether sialic acid (SIA) existed in the inflammatory exudate of the carrageenin (Car)-air pouch model and to elucidate the mechanisms of the antiinflammatory action of SIA on the Car-induced edema in rat hind paws. SIA (113.20 +/- 10.73 micrograms/ml) was detected in the exudate of Car-air pouch, and the plasma SIA (660.29 +/- 29.38 micrograms/ml) in Car-air pouch rats was significantly higher than that (490.00 +/- 29.37 micrograms/ml) in control rats. SIA (300 mg/kg, s.c.) suppressed the delayed phase of Car-induced edema, and it also suppressed the edema induced by Car plus arachidonic acid, Car plus PGE2, and bradykinin plus PGE2. However, SIA did not affect the edema induced by dextran, histamine, bradykinin, and Car plus PGE1. SIA affected neither the PG production in rats nor the [3H]PGE2-receptor binding of guinea pig ileum, and SIA reduced the PGE2-induced contraction of isolated guinea pig ileum. The above results suggest that SIA induces the antiinflammatory effects via its antagonism against PGE2. Furthermore, the presence of SIA in the inflammatory exudate and the higher concentration of SIA in the plasma than in the exudate might suggest that SIA plays patho-physiologically protective roles in inflammatory states.

Animals↗

Afferent innervation of the gallbladder in the cat, studied by the horseradish peroxidase method.

Following injection of horseradish peroxidase (HRP) into the wall of the gallbladder of cats, HRP-positive cells were found bilaterally in dorsal root ganglia T2-L3 (T2-L2, and T3-L2/L3 also observed in a few cats) and nodose ganglia. In about 33% of animals labelled cells were also distributed in cervical dorsal root ganglia C5-C7. Labelled cells were more frequently localized on the right side than the left. There was no apparent change in numbers of labelled cells in the nodose ganglion (NG) on either side following greater and lesser splanchnicotomy or section of the right phrenic nerve or removal of the celiac ganglion. After severing both the greater and lesser splanchnic nerves unilaterally, numbers of labelled afferent cells from the gallbladder in dorsal root ganglia (DRGs) significantly decreased on the ipsilateral side but there was no change in the pattern of distribution contralaterally. After section of the right phrenic nerve, labelled cells were not found in ipsilateral cervical ganglia. That some afferent fibers from the gallbladder travel via the phrenic nerves, particularly on the right side, may be a supplementary mechanism in the generation of referred pain in gallbladder disease. The splanchnic nerves are the main, but not the only pathway for afferent fibers from the gallbladder.

Afferent Pathways↗

Induction of kinetic cell death and its underlying mechanisms.

Using a modified Langendorff system, we established an experimental model of kinetic cell death in the rat heart. After calcium (5.5 mM) was loaded for 20 min and 10(-7) mol isoproterenol was then delivered to the perfusion medium, the hearts developed tonic contracture. Histological examination of the myocardium revealed widespread kinetic cell death. Stimulation of alpha-adrenoceptors with phenylephrine did not induce kinetic cell death, even after calcium loading. In our kinetic cell death model in the rat, the outflow of creatine phosphokinase into the perfusion medium was increased after isoproterenol application, with a peak occurring at 45 min. The peak transient increase in the intracellular calcium ion concentration (the Ca-transient) was measured using Fura2/AM, and was found to be augmented by increasing the calcium concentration of the perfusion medium. These results suggest that in the presence of an increased intracellular calcium concentration, even slight stimulation of beta-adrenoceptors can easily induce myocardial injury.

Animals↗

Interleukin-2 receptor antigen, leukocyte common antigen, and Ki-1 antigen-expressing gastric plasmacytoma. A case report with an immunohistochemical study.

A case of primary gastric plasmacytoma expressing various surface and cytoplasmic antigens is reported. With the use of formalin-fixed and deparaffinized sections, 13 different antibodies were applied. Neoplastic plasma cells revealed monoclonal IgG and kappa light chain in the cytoplasm, and expressed epithelial membrane antigen, Ki 67 antigen, cytokeratin, CD 22 antigen, interleukin-2 receptor antigen, leukocyte common antigen and Ki-1 (CD 30) antigen. However, tumor cells were devoid of HLA-DR antigen. These data suggest that the neoplastic plasma cells are at the plasmoblastic stage of maturation and express various surface and cytoplasmic phenotypes.

Aged↗

Inhibitory effect of extracts of muscles of mackerel (Scomber japonicus Houttuyn) on hepatic glycogenolysis in rats.

The effects of extracts of muscles of mackerel (Scomber japonicus; M-ext) on hepatic glycogenolysis were investigated by a rat liver perfusion method. M-ext inhibited glucagon- and cyclic adenosine monophosphate (AMP)-induced glycogenolysis but was ineffective on phenylephrine-induced glycogenolysis. The contents of hepatic glycogen and cyclic AMP, and phosphorylase and glycogen synthase activities in liver were measured after perfusion with glucagon. M-ext inhibited the increase of cyclic AMP and activation of phosphorylase. It is considered that M-ext inhibits hepatic glycogenolysis caused by glucagon through a cyclic AMP-dependent mechanism.

Animals↗

Myoblast-mediated fusion-injection: a new technique for introduction of macromolecules specifically into living skeletal muscle cells.

A new technique for the introduction of macromolecules specifically into living skeletal muscle cells has been developed by a modification of the red blood cell ghost-mediated fusion-injection technique [M. Furusawa (1980) Int. Rev. Cytol. 62, 29-67]. Fluorescein-labeled bovine serum albumin (FITC-BSA) was introduced into chicken skeletal muscle myoblasts by the human red blood cell-mediated fusion-injection method in the presence of polyethylene glycol. Myoblasts loaded with FITC-BSA were then purified by a fluorescence cell sorter and cocultured with myotubes. Specific cell fusion between myoblasts and myotubes occurred under normal culture conditions and BSA was successfully introduced into living myotubes. This technique may provide a new method not only for the study of a given macromolecule's function in living muscle cells but also for therapeutic purposes such as muscle-specific drug delivery.

Animals↗