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Biomedical subjects

S Matsuo

Publications and source records attributed to S Matsuo.

At least 199 records · Page 11Linked to original sources
PubMed1995

Flow cytometric analysis of pig epidermal keratinocytes: effects of ultraviolet B irradiation (UVB) and topical PUVA treatment.

The effects of a single application of ultraviolet B irradiation (UVB) and topical PUVA treatment on pig epidermal cell kinetics were studied by DNA-flow cytometry (FCM), 3H-thymidine uptake, mitotic counts and 2-3H-deoxy-D-glucose uptake. Following UVB irradiation (2MED: 250 mJ/cm2) and PUVA (0.9, 1.4 J/cm2) treatment, thymidine uptake and mitosis were markedly decreased. This was followed by a transient increase in all of these parameters. The maximal increase was observed at 96 h following the UVB irradiation and at 168 h following the PUVA treatment (0.9 J/cm2), respectively. The suppression of DNA synthesis and mitosis persisted for a longer period in PUVA-treated than in UVB-treated epidermis. At 48-72 h after the UVB irradiation and 72-144 h after the PUVA treatment, an increase in the cells of the G2/M fraction was observed. This was associated with the decreased mitotic counts, suggesting accumulation of G2-blocked cells. Histologically, PUVA-treated epidermis showed a considerable degenerative change. Mild acanthosis was noted at 72-96 h in UVB-treated epidermis and at 168 h in PUVA-treated epidermis. These results indicate that the inhibition of DNA synthesis and increase in G2-phase cells are associated with the UVB and PUVA induced suppression of epidermal cell proliferation. These suppressive effects that persisted longer in PUVA-treated, than in UVB-treated epidermis, were followed by an increased epidermal keratinocyte proliferation of pig skin in vivo.

Animals↗
PubMed1995

Topical tacalcitol (1,24-(R)-dihydroxyvitamin D3) induces a transient increase in thymidine incorporation and calmodulin content in pig epidermis following tape stripping in vivo.

Tape stripping induces transient increase in keratinocyte proliferation in vivo. The effects of tacalcitol (1,24-(R)-dihydroxyvitamin D3) ointment on the cell kinetics of pig epidermis after the tape stripping were investigated. The tacalcitol ointment (2 micrograms/g) was applied once to the back of pigs immediately after the tape stripping. The pig epidermal cell kinetics were analyzed at various times following the treatment. Tape stripping transiently increased thymidine incorporation of keratinocytes; the maximal effect was observed at 24 h. Tape stripping-induced increase in thymidine incorporation was markedly augmented by tacalcitol treatment. At 24 h following the tape stripping DNA-flow cytometry revealed an accelerated transition from G0/1 to S phase of cell cycle in tacalcitol treated epidermis. There was no significant difference, however, in mitotic counts and G2/M phase fractions between tape stripping-treated and tape stripping plus tacalcitol ointment-treated epidermis. We also measured calmodulin content of pig epidermis following the treatments. Although tape stripping slightly increased calmodulin content of pig epidermis, this was statistically not significant. Tape stripping plus tacalcitol ointment treatment resulted in a significant increase in calmodulin content at 24 h following the treatment. There was no significant difference in calmodulin content between tape stripping treated- and tape stripping plus tacalcitol-treated epidermis.

Administration, Topical↗
PubMed1995

Degradation of macromolecules during preservation of lyophilized pathological tissues.

Methods of preserving biological specimens are becoming more important due to recent advances in molecular biological analysis. Storing samples in a freezer, however, is still the most commonly used method of preserving pathological specimens. We investigated the feasibility of using freeze-dried tissues stored at room temperature as an alternative method of preserving tissue samples for molecular analysis at the DNA, RNA, and protein levels. The freeze-dried tissues were transferred to a sealed vial filled with nitrogen gas and kept for months at room temperature. DNA and protein were stably preserved for at least 24 weeks. RNA, however, showed slight degradation after 10 weeks of storage. Controlling moisture and temperature during long-term storage was found to be important, as it significantly affected the stability of these cellular molecules in tissues. Shelf-stable preservation eliminates the need for storage in a freezer and allows convenient shipping of samples to distant places. These findings should provide practical basis for the development of a convenient and economical way of preserving pathological specimens for a variety of analyses in the field of molecular biology.

Animals↗
PubMed1995

Role of a rat membrane inhibitor of complement in anti-basement membrane antibody-induced renal injury.

In the kidneys of anti-glomerular basement membrane (anti-GBM) antibody disease, binding of antibodies to tubular basement membrane (TBM) is often observed. The present work was performed to explore the mechanisms of binding of anti-GBM antibodies to TBM in vivo with special reference to 5I2Ag, a rat membrane inhibitor of complement which regulates complement activation at C3 convertase level. To suppress functions of renal 5I2Ag, F(ab')2 fragment of 5I2 (a neutralizing mAb against 5I2Ag) was perfused in the left kidney and then blood circulation was restored. Mild proteinuria ( < 10 mg/16 hr) was observed during first several days. Five days later, there were tubulointerstitial injuries defined by tubular vimentin staining and leukocyte infiltration. Significant deposition of C3 was observed in the capillaries and in TBM. In rats intravenously injected with rabbit anti-rat GBM antibodies five minutes after kidney perfusion with 5I2, strong binding of rabbit IgG to TBM was observed at one and five days after injection. Although these rats showed mild proteinuria comparable to those perfused with 5I2 and those injected with normal rabbit serum, tubulointerstitial injury was significantly enhanced at Day 5. In contrast, rats perfused with irrelevant mAb and injected with anti-GBM antibodies did not show any significant binding of antibodies to TBM nor tubulointerstitial injury. Furthermore, rats which were made proteinuric by puromycin aminonucleoside and injected with anti-GBM antibodies did not show any significant binding of rabbit IgG to TBM. These results indicate that 5I2Ag, a rat membrane inhibitor of complement at the C3 convertase level, regulates vascular permeability in the living kidney, and that dysfunction or decreased expression of this molecule leads to increased accessibility of anti-GBM antibodies to TBM.

Albuminuria↗
PubMed1995

Interferon-gamma-dependent stimulation of Fas antigen in SV40-transformed human keratinocytes: modulation of the apoptotic process by protein kinase C.

Fas antigen is a cell membrane protein that has been suggested to mediate apoptosis. Using SV40-transformed human keratinocytes, we investigated the Fas-antigen-dependent apoptotic process. The expression of Fas antigen mRNA was markedly induced by interferon-gamma (IFN-gamma) treatment (500 U/ml). After IFN-gamma treatment in the presence of anti-Fas monoclonal antibody, apoptosis was induced, as detected by the formation of nucleosome-sized fragments of DNA and morphologically by apoptotic cells with round homogeneous nuclear beads detected by acridine orange staining. The apoptotic SV40-transformed keratinocytes were analyzed quantitatively by enzyme-linked immunosorbent assay using antihistone and peroxidase-conjugated anti-DNA antibodies to detect cell death. The IFN-gamma- and anti-Fas antibody-dependent apoptotis was observed by 3 h, and the maximal response was observed by 12 h. The induction of apoptosis was significantly augmented by treatment with 10 ng/ml 12-o-tetradecanoyl-phorbol-13-acetate (TPA). TPA alone had no effect on either Fas antigen expression or on the apoptotic process. Other protein kinase C activators (1-oleoyl-2-acetylglycerol and mezerein) also stimulated IFN-gamma-dependent apoptosis, whereas 4-o-methyl phorbol myristate acetate, a very weak protein kinase C activator, had only a slight effect. The TPA-induced augmentation of apoptosis was inhibited by the protein kinase C inhibitor, 1-(5-isoquinoline-sulfonyl)-2-methyl piperazine dihydrochloride (H-7). However, H-7 inhibited only the TPA-induced augmentation of apoptosis; the basal IFN-gamma- and anti-Fas-dependent apoptosis remained in the presence of H-7. Northern blot analysis revealed that c-jun mRNA was induced by IFN-gamma plus anti-Fas antibody treatment as well as by TPA treatment; the addition of IFN-gamma alone to the incubation medium had no effect on the expression of c-jun mRNA. These results indicate that IFN-gamma induces a Fas-antigen-dependent apoptotic process in SV40-transformed keratinocytes and that TPA augments the process through the activation of protein kinase C.

Apoptosis↗
PubMed1995

Lyme disease in Japan. Analysis of Borrelia species using rRNA gene restriction fragment length polymorphism.

BACKGROUND: Lyme disease is sporadically observed in Japan since the first report in 1987. We have experienced 19 cases of Lyme disease. In 12 out of 13 trials we succeeded in isolating Borrelia strains (JEM1-12) from erythema migrans (EM) lesions. Recently, Borrelia burgdorferi sensu lato was classified into at least three distinct subgroups, B. burgdorferi sensu stricto, B. garinii and B. afzelii. OBJECTIVE: In order to characterize Lyme disease in Japan, we summarized the clinical features of our cases and investigated the nature of the isolated Borrelia strains. METHODS: The 12 Borrelia strains were analyzed by restriction fragment length polymorphism (RFLP) of ribosomal RNA gene. RESULTS: Most of our 19 patients were in stage I with EM as the main clinical manifestation. RFLP analysis using 12 strains isolated from the patients indicated that 8 strains (group IV, V) were different from the three aforementioned genospecies. CONCLUSION: Clinical data from the present study substantiate the view that Japanese Lyme disease has a relatively milder course. We speculate that this may be related to the specific Borrelia strains in Japan.

Adult↗
PubMed1995

Tubulointerstitial injury induced in rats by a monoclonal antibody that inhibits function of a membrane inhibitor of complement.

The kidney widely expresses membrane-associated complement regulatory proteins (membrane inhibitors of complement). The aim of this work was to evaluate the roles of these molecules in rat kidneys in vivo. To suppress functions of rat membrane inhibitors of complement, two mAbs, 512 and 6D1, were used. 5I2 and 6D1 inhibit functions of membrane inhibitors of complement at C3 level (rat Crry/p65) and C8/9 level (rat CD59), respectively. F(ab')2 fragment of 5I2 or 6D1 was perfused in the left kidneys, and perfusate was discarded from the renal vein. After perfusion, the left kidneys were connected to systemic circulation. In rats perfused with 5I2, mouse IgG was found in glomeruli, peritubular capillaries, vascular bundles, and tubules 15 min after recirculation. Binding of C3 and C5b-9 was evident in these areas. 1 d after perfusion with 5I2, cast formation, dilatation of tubular lumen, and tubular cell degeneration were observed. At day 4 through day 7, significant mononuclear cell infiltration and proximal tubule damage were observed. These changes were completely prevented by complement depletion. Rats perfused with 6D1 showed the binding of mouse IgG in the similar areas as 5I2, but C3 or C5b-9 deposition was not observed. Rats perfused with 6D1 or vehicle only did not show any pathology in the left kidneys. These results suggest that rat Crry/p65 plays protective roles against spontaneously occurring indiscriminate attack to tubulointerstitial tissues by autologous complement and that rat Crry/p65 is one of the important factors to maintain normal integrity of the kidney in rats.

Animals↗
PubMed1995

The role of a complement regulatory protein in rat mesangial glomerulonephritis.

The host cells are protected from the indiscriminate attack of homologous complement by the membrane-associated complement regulatory proteins. A mouse monoclonal antibody (mAb) 512 (immunoglobulin G1 subclass) has recently been described that recognizes and inhibits the function of a rat complement regulatory protein, a rat homologue of mouse Crry/p65. The aim of this work is to assess the role of a complement regulatory protein (512Ag) recognized by mAb 512 in the complement-dependent glomerular injury induced by mAb OX7 against rat Thy-1.1. For the induction of mesangial injury, the left kidney of a rat was perfused with a combination of OX7 and 512 and the perfusate was discarded from the renal vein (Group I). After the renal artery and vein were restored, the left kidney was connected to the systemic circulation. Rats were euthanized 3 h, 2 days, and 14 days later. Rats perfused either with OX7 (Group II) or with 512 (Group III) or with vehicle only (Group IV) were used as controls. At 3 h, rats of Group I showed more prominent cellular infiltration and mesangial lysis and more C3 deposition in the glomeruli than rats of Group II. Rats of Groups III and IV showed no significant changes. At Day 2, there was still significant mesangial lysis and leukocyte infiltration in Group I rats, whereas rats in other groups showed an almost normal appearance. Glomerular injury in Group I rats returned to normal by Day 14.

Animals↗
PubMed1995

Posterior canal-activated excitatory vestibuloocular relay neurons participate in the vestibulocortical pathways in cats.

We have previously reported that axon collaterals of posterior canal-activated excitatory vestibular (PC) neurons project to the contralateral oculomotor nucleus, and rostrally to the thalamus. To elucidate the vestibulothalamocortical pathways we investigated the synaptic connections of the PC neurons with the thalamic neurons by post-spike averaging of compound potentials triggered by spikes of the PC neuron in anesthetized cats. The averaged field potential evoked in the ventrobasal complex (VBC) revealed a spike followed by a negative wave. Latencies of the wave ranged from 0.8 to 1.5 ms. Next, we examined the location and axonal projection of 36 thalamic neurons which were activated by nose-up head rotation and by contralateral labyrinth stimulation. Most of them were located in the VBC and some in the medial geniculate body. Thirteen of the 36 neurons were antidromically activated from the anterior suprasylvian sulcus or postcruciate dimple of the cortex. These results suggest that the PC neurons participate, at least in part, in the vestibulocortical pathways contributing to spatial orientation.

Animals↗
PubMed1995

A case of bullous pemphigoid with antibodies against intercellular 130 kd antigen.

Pemphigus and bullous pemphigoid are two typical autoimmune bullous diseases that involve circulating autoantibodies directed against the epidermal cell surface and the epidermal basement membrane zone, respectively. The coexistence of pemphigus and bullous pemphigoid is rare. We describe a case of a 79-year-old man who had tense bullae and erythematous, erosive lesions on his trunk and four extremities. Histopathology revealed subepidermal blister formation without any evidence of intraepidermal acantholytic changes. Direct immunofluorescence study demonstrated deposition of IgG on the epidermal intercellular spaces, as well as along the basement membrane zone; C3 was detected only on the latter. Indirect immunofluorescence study using monkey esophagus as a substrate demonstrated the presence of circulating antibodies against both junctional and intercellular antigens. In order to analyze the precise nature of this patient's antibodies, indirect immunofluorescence study using cultured human keratinocytes and immunoblot analyses were performed. Pemphigus vulgaris sera showed smooth and uniform staining on intercellular spaces. The patient's serum showed a granular and uneven staining pattern. Immunoblot analysis showed that the patient's serum reacted with the typical 230 kd (bullous pemphigoid) antigen and 130 kd antigen, which is close to the pemphigus vulgaris antigen.

Aged↗
PubMed1995

Interaction of antibody with Forssman antigen in guinea pigs. A mechanism of adaptation to antibody- and complement-mediated injury.

Forssman antigen is a glycosphingolipid with antigenic specificity determined by extra-membrane haptenic sugars similar to blood group antigens and antigens that are the main barrier to xenogeneic organ transplantation. Herein, we describe the localization of Forssman antigen in guinea pig lungs and kidneys and the consequences of its interaction with antibodies in vitro and in vivo (Forssman reaction). Exposure of cultured guinea pig aortic endothelial cells to Forssman antibodies induced rapid redistribution of antigen-antibody complexes at the cell surface, followed by shedding that occurred by blebbing of plasma membrane as vesicles or fragments, and was associated with disappearance of antigen from the cell surface (antigenic modulation). Guinea pigs surviving frequent intravenous infections of increasing amounts of antibodies, for a total of 20 to 40 lethal doses, developed a partial or complete adaptation to generalized Forssman reaction, and adaptation was associated with partial or complete modulation of Forssman antigen at the surface of the pulmonary and, in minor degree, renal endothelial and epithelial cells. These findings support the hypothesis that modulation of endothelial carbohydrate antigens contributes to adaptation of highly vascularized organs exposed to tolerable levels of allo- or xenoantibodies.

Animals↗
PubMed1995

In vivo effects of hyperglycemia on the outcome of acute mesangial injury in rats.

To assess the effects of high blood glucose concentration on glomerular changes after the acute mesangial cell injury in the rat, the monoclonal anti-Thy1.1 antibody OX-7 was injected into streptozoticin-induced diabetic rats or normal rats. The increase in proliferating cell nuclear antigen-positive cells in glomeruli at day 4 and glomerular hypercellularity at day 18 was less prominent in diabetic rats than in normal rats. The expansion of mesangial matrix area assessed by fibronectin immunostaining was more prominent, and segmental glomerulosclerosis was observed at day 60 in the diabetic rats. These data suggest that the insulin-deficient group may reflect impaired "wound-healing," leading to the prolonged ECM accumulation under the hyperglycemic condition in vivo.

Acute Disease↗
PubMed1994

In vivo effects of monoclonal antibodies that functionally inhibit complement regulatory proteins in rats.

The present work was designed to evaluate the effects of functional suppression of complement regulatory proteins in vivo. Male Wistar rats were anesthetized with Nembutal and were intravenously injected with 1 mg/kg of F(ab')2 or Fab fraction of either monoclonal antibody 5I2, which inhibits the function of rat counterpart of mouse Crry/p65, or monoclonal antibody 6D1, which inhibits the rat counterpart of CD59. Mean arterial pressure was continuously measured for 30 min. When 5I2 was injected, there was a biphasic change of mean arterial pressure, namely, the rapid increase immediately after the injection (approximately 2 min, phase 1) and the subsequent fall and slow recovery (approximately 4-30 min, phase 2). These effects were completely abrogated by pretreatment of rats with cobra venom factor. Pretreatment with carboxypeptidase inhibitor, which inhibits inactivation of anaphylatoxins C3a and C5a, induced enhanced reduction of blood pressure. Circulating leukocytes and platelets were rapidly decreased 5 min after antibody injection and became normal by 2 h. Hematocrit and erythrocyte count were continuously increased up to 2 h after injection, suggesting that there was hemoconcentration due to increased vascular permeability. Immunofluorescence study revealed binding of antibody fragments and rat C3 along the capillaries of lung, heart, and liver 5 min after injection. In contrast to 5I2, F(ab')2 fraction of 6D1, though localized to the same areas and in similar amounts, had no significant effect on the parameters measured. These data suggest that the rat counterpart of mouse Crry/p65 plays a vital role in vivo by preventing the activation of autologous complement on vascular endothelium.

Animals↗
PubMed1994

Medium-lead burst neurons related to vertical saccades in cat Forel's field H: input from vestibular nucleus.

The present study was undertaken to investigate synaptic connections between medium-lead burst neurons (MLBNs) related to vertical saccades in Forel's field H and vestibular nucleus (VN) neurons. Extracellular spikes were recorded from single MLBNs and their responses to VN stimulation were examined using chronically prepared alert cats. Twenty of 30 upward MLBNs and 10 of 22 downward MLBNs could be synaptically activated mainly by the ipsilateral VN stimulation with spike latencies of 2.2-12.0 and 1.9-11.7 ms, respectively. These results suggest that there exist di- or polysynaptic connections which transfer velocity signals for vertical saccades from the ipsilateral vestibular nucleus neurons to the vertical MLBNs.

Animals↗