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Seiichi Matsuo

Publications and source records attributed to Seiichi Matsuo.

At least 19 recordsLinked to original sources
PubMed2006

Comparison of percutaneous coronary intervention with medication in the treatment of coronary artery disease in hemodialysis patients.

It has been reported that percutaneous coronary intervention (PCI) is beneficial for coronary artery disease (CAD) among the general population. However, its effects in patients who are on hemodialysis (HD) remain unclear. A prospective cohort study was performed to clarify whether PCI has a therapeutic advantage over medical therapy among HD patients with CAD. A follow-up study to 5 yr was conducted among 259 HD patients with ischemic heart disease. Mean follow-up was 39 mo. Patients were divided into three groups: 122 patients without significant stenosis, 88 patients who had significant stenosis and were treated with PCI, and 49 patients who had significant stenosis and were treated with medication only. The primary end point was cardiac death, and the secondary end point was all-cause death. The results showed that the 5-yr cardiac survival rate was 41.6% in the medication group, 77.1% in the PCI group (P = 0.0006), and 84.5% in the nonstenosis group (P < 0.0001). The 5-yr all-cause survival rate was 19.3% in the medication group, 48.4% in the PCI group (P = 0.004), and 64.3% in the nonstenosis group (P < 0.0001). Even after adjustment for other risk factors, effects of PCI on the risk for cardiac and all-cause death remained significant and independent (odds ratio 0.14; 95% confidence interval 0.08 to 0.25, P = 0.0006; and odds ratio 0.37; 95% confidence interval 0.26 to 0.54, P = 0.0062, respectively). Results were consistent when the therapeutic effect of PCI or medication was analyzed using propensity-matched patients. These data suggested that PCI could improve the prognosis of HD patients with CAD. PCI would be recommended for HD patients with CAD.

Aged↗
PubMed2006

Effects of low molecular weight heparin on the frequencies of intradialytic arrhythmias in hemodialysis patients.

Arrhythmia is known to cause sudden death in hemodialysis patients. Heparin administration releases lipoprotein lipase from the capillary endothelial cell surface, resulting in an increase in the plasma levels of free fatty acids; higher levels of free fatty acids may affect the occurrence of arrhythmias. This study assessed whether the occurrence of arrhythmias during hemodialysis could be suppressed by replacing unfractionated heparin with low molecular weight heparin. Ten dialysis patients who had supraventricular premature contraction and/or ventricular premature contraction were monitored by the Holter electrocardiograph system during hemodialysis. To investigate the effect of each form of heparin on plasma lipid metabolism, the lipoprotein lipase and lipid levels before and during hemodialysis were measured. The occurrence of arrhythmias was significantly suppressed in hemodialysis using low molecular weight heparin, as compared with hemodialysis using unfractionated heparin. Lower lipoprotein lipase and free fatty acids levels were also observed in hemodialysis using low molecular weight heparin. The authors concluded that hemodialysis using low molecular weight heparin instead of unfractionated heparin could be effective in protecting hemodialysis patients with arrhythmias against arrhythmia-related cardiac events.

Antifibrinolytic Agents↗
PubMed2006

Growth factor midkine is involved in the pathogenesis of diabetic nephropathy.

Diabetic nephropathy is a life-threatening disease associated with diabetes mellitus. Longstanding hyperglycemia induces pathological reactions of glomerular mesangial cells, such as overproduction of extracellular matrix, which finally lead to nephropathy. However, the mechanisms underlying its pathogenesis have not been completely elucidated. Using the Streptozotocin-induced model of diabetes, we report that mice deficient in the growth factor midkine (Mdk-/-) exhibited strikingly milder nephropathy than Mdk+/+ mice, even though both mice showed similar extents of hyperglycemia after Streptozotocin injection. Midkine expression was induced in the glomerular mesangium of Mdk+/+ mice with diabetic nephropathy and in primary cultured mesangial cells exposed to high glucose. Mdk-/- mesangial cells exhibited reduced phosphorylation of protein kinase C and extracellular signal-regulated kinase as well as reduced production of transforming growth factor-beta(1) on high glucose loading. Addition of exogenous midkine restored extracellular signal-regulated kinase phosphorylation in Mdk-/- cells under high glucose conditions, whereas a midkine antisense oligodeoxynucleotide suppressed midkine in Mdk+/+ cells. Therefore, this study identifies midkine as a key molecule in diabetic nephropathy and suggests that midkine accelerates the intracellular signaling network evoked by hyperglycemia in nephropathy.

Animals↗
PubMed2005

GDNF-inducible zinc finger protein 1 is a sequence-specific transcriptional repressor that binds to the HOXA10 gene regulatory region.

The RET tyrosine kinase receptor and its ligand, glial cell line-derived neurotrophic factor (GDNF) are critical regulators of renal and neural development. It has been demonstrated that RET activates a variety of downstream signaling cascades, including the RAS/mitogen-activated protein kinase and phosphatidylinositol-3-kinase(PI3-K)/AKT pathways. However, nuclear targets specific to RET-triggered signaling still remain elusive. We have previously identified a novel zinc finger protein, GZF1, whose expression is induced during GDNF/RET signaling and may play a role in renal branching morphogenesis. Here, we report the DNA binding property of GZF1 and its potential target gene. Using the cyclic amplification and selection of targets technique, the consensus DNA sequence to which GZF1 binds was determined. This sequence was found in the 5' regulatory region of the HOXA10 gene. Electrophoretic mobility shift assay revealed that GZF1 specifically binds to the determined consensus sequence and suppresses transcription of the luciferase gene from the HOXA10 gene regulatory element. These findings thus suggest that GZF1 may regulate the spatial and temporal expression of the HOXA10 gene which plays a role in morphogenesis.

Animals↗
PubMed2005

A useful new classification of dysmorphic urinary erythrocytes.

BACKGROUND: Among dysmorphic urinary erythrocytes (D cells), G1 cells or doughnut-shaped erythrocytes with one or more blebs are considered to be reliable markers for glomerular diseases. However, although there are many D cells with cytoplasmic color loss and without blebs in the urinary sediment, the significance of these cells is not clear. In this study, we devised a classification system for D cells and examined the relation between these cell types and urinalysis data. METHODS: We classified D cells into three types (D1, D2, and D3 cells): D1 cells showed a ring-like shape and severe loss of cytoplasmic color with protrusions or blebs; D2 cells showed a doughnut-like shape and moderate cytoplasmic color loss with protrusions or blebs; and D3 cells showed a doughnut-like shape and mild cytoplasmic color loss without protrusions or blebs. We calculated the numbers of D cells of each type in 45 patients with glomerular diseases and in 303 general outpatients. This was done by bright-field microscopy modified for the analysis of urinary sediment, and we also examined the significance of these cell types. RESULTS: In the 45 patients with glomerular diseases, the numbers of D1, D2, and D3 cells correlated with urine levels of proteinuria and hematuria and numbers of cellular and fatty casts. Numbers of D1 and D2 cells correlated with urine concentrations of albumin and N-acetyl-beta-D-glucosaminidase, and the proportions of D1 and D2 cells in D cells increased with the activity of glomerular diseases classified by urinalysis data. Only the number of D1 cells correlated with the urine concentration of potassium, which may increase in hemolysis. In the 303 outpatients, the sensitivity of D3 cells and D1 and/or D2 cells (G1 cells) was 73% and 46%, respectively, for the detection of glomerular diseases and the specificity was 93% and 99%, respectively. CONCLUSIONS: These data indicate that the D3 cell is a sensitive marker for glomerular diseases, and that D1 and/or D2 cells are markers for severe glomerular diseases.

Acanthocytes↗
PubMed2005

Midkine antisense oligodeoxyribonucleotide inhibits renal damage induced by ischemic reperfusion.

BACKGROUND: Midkine, a heparin-binding growth factor, is involved in the migration of inflammatory cells. The inflammatory cell migration to the tubulointerstitium of the kidney after ischemia/reperfusion (I/R) injury is attenuated in midkine gene-deficient mice, resulting in better preservation of the tubulointerstitium compared with wild-type mice. In the present investigation, we planned to evaluate the usefulness of antisense midkine for the therapy of ischemic renal failure. METHODS: Midkine antisense phosphorothioate oligodeoxyribonucleotide (ODN) at a dose of 1 mg/kg in saline was intravenously administered to mice 1 day before or after I/R. The kidneys were removed for examination 1, 2, 3, and 7 days after I/R. RESULTS: It was rapidly incorporated into proximal tubular epithelial cells, and inhibited midkine synthesis, leading to reduced migration of inflammatory cells to the injured epithelial layer. Consequently, the midkine antisense ODN-treated animals exhibited less severe renal damage than untreated or midkine sense ODN-treated animals 2 days after I/R as assessed by morphologic criteria and blood urea nitrogen (BUN) and serum creatinine levels. Midkine expression, BUN, and serum creatinine levels were not significantly different between injection of midkine antisense ODN before and after ischemic injury. CONCLUSION: These results indicate that intravenous injection of midkine antisense ODN is a candidate for a novel therapeutic strategy against acute tubulointerstitial injury induced by I/R injury.

Animals↗
PubMed2005

Geranylgeranylacetone ameliorates ischemic acute renal failure via induction of Hsp70.

BACKGROUND: Heat shock proteins (HSPs) are well known as cytoprotective proteins. Geranylgeranylacetone (GGA), an antiulcer agent, has recently been shown to induce Hsp70. This study was performed to investigate the renoprotective properties of GGA. METHODS: The effect of GGA on the induction of the major HSPs (Hsp90, Hsp70, Hsc70, Hsp60, and Hsp32) was studied in the rat kidney or rat primary cultures of tubular epithelial cells (R-TECs) by Western blot. Localization of Hsp70 was determined by immunohistochemistry. The renoprotective effects of GGA were studied using a rat model of ischemia/reperfusion (I/R) injury. GGA (400 mg/kg), GGA with quercetin pretreatment (100 mg/kg), or a vehicle was given to rats 24 hours and again 1 hour prior to the induction of I/R injury. Rats were sacrificed at 24 hours after reperfusion. Histologic analyses and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL) assay were performed. Blood urea nitrogen (BUN) and serum creatinine was also measured. The cytoprotective properties of GGA were also studied in vitro by treating R-TECs with GGA (10 mumol/L) or a vehicle, followed by incubation in culture medium with oxidative stress condition (0.5 mmol/L hydrogen peroxide) or ischemic condition (2 nmol/L NaCN and 20 mmol/L 2-deoxyglucose in the absence of medium glucose). RESULTS: Oral administration of GGA induced Hsp70 expression in the kidney (which peaked at 24 hours) but did not induce Hsp90, Hsc70, Hsp60, or Hsp32. The induction of Hsp70 was blocked by quercetin. Immunohistochemistry showed that Hsp70 was localized mainly in the tubular epithelial cells. Preconditioning rats with GGA significantly decreased BUN and serum creatinine levels after I/R injury. Histologic examination revealed that GGA significantly attenuated tubular damage and macrophage infiltration. The number of TUNEL-positive cells also decreased significantly in the GGA group. Quercetin, an inhibitor of Hsp70 induction, eliminated these renoprotective effects of GGA. In in vitro study, GGA-induced Hsp70 in R-TECs, which peaked at 2 to 4 hours. Both oxidative stress and ischemic stimuli induced apoptosis in R-TECs. GGA significantly suppressed the number of apoptotic cells in both conditions. CONCLUSION: The results support the hypothesis that GGA induces Hsp70, protects tubular epithelial cells from apoptosis, and thus ameliorates tubular damage by I/R injury. The present study suggests that GGA would be a useful tool in treating acute renal failure or preventing transplanted kidney damage in the clinical setting.

Acute Kidney Injury↗
PubMed2005

Fish mesonephric model of polycystic kidney disease in medaka (Oryzias latipes) pc mutant.

BACKGROUND: Polycystic kidney disease (PKD) is a common hereditary disease. A number of murine and zebrafish mutants have been generated and used for the study of PKD as metanephric and pronephric models, respectively. Here, we report a medaka (Oryzias latipes) mutant that develops numerous cysts in the kidney in adulthood fish in an autosomal-recessive manner as a mesonephric model of PKD. METHODS: The phenotypes of the medaka pc mutant were described in terms of morphologic, histologic, and ultrastructural features. The pc see-through stock was produced by crossing a pc mutant and a fish from the see-through stock and used for observing the kidney through the transparent body wall of a live fish. RESULTS: The mutant developed bilateral massive enlargement of the kidney in adulthood. They sexually matured normally within 2 months of age and died within 6 months of age. The affected kidney was occupied by numerous, fluid-filled cysts, which were lined by attenuated squamous epithelial cells. Developmentally, cystic formation began in the pronephros in 10-day-old fry and in the mesonephros in 20-day-old fry at the microscopic level. The pc see-through stock was useful in observing disease progression in live fish. CONCLUSION: The kidney disorder that develops in the medaka pc mutant is a mesonephric counterpart of PKD, particularly an autosomal-dominant PKD, based on its morphologic, histologic, and ultrastructural features, and slow progression.

Animals↗
PubMed2005

Shiga toxin 1 causes direct renal injury in rats.

Infection with Shiga toxin (Stx)-producing Escherichia coli has been implicated to cause hemolytic uremic syndrome, which is characterized by histological abnormalities such as microvascular thrombi and tubular cell damage in the kidney. Although Stx is known to be the major virulence factor of the pathogen, it is still unclear whether Stx directly impairs renal cells in vivo to cause such histological changes and deterioration of renal function. To assess the consequence of the direct action of Stx on renal cells, left kidneys of rats were perfused with Stx1 from the renal artery through the renal vein and then revascularized. Kidneys of control animals were perfused with the vehicle alone. On day 1, apoptosis and induction of tumor necrosis factor alpha gene expression were noticed to occur in the medulla of the Stx1-perfused kidneys. On day 3, extensive tubular injuries were observed by light microscopy: aggregated platelets and monocytic infiltrates in both glomeruli and the medullary interstitium were detected by immunostaining. Tubular changes were more extensive on day 9, with areas of infarction seen in the cortex and medulla. These changes were not found to occur in the sham-operated kidneys. No obvious glomerular changes were detected by light microscopy at any time point. When nonperfused right kidneys were removed after the Stx1 perfusion of the left kidneys, the serum creatinine and blood urea nitrogen levels were increased from day 2, and acute renal failure followed on day 3. These results indicate that Stx1 caused glomerular platelet aggregation, tubular damage, and acute deterioration of renal function by acting directly on renal cells.

Animals↗
PubMed2005

Therapeutic neovascularization using cord blood-derived endothelial progenitor cells for diabetic neuropathy.

Diabetic neuropathy is based on the impairment of nerve blood flow and the metabolic disorder. Although the vasodilating agents and anticoagulants improve nerve function and symptoms in diabetic neuropathy, more effective treatments are needed. Because endothelial progenitor cells (EPCs) have been identified in adult human peripheral blood, many studies have shown that transplantation of EPCs improves circulation to ischemic tissues. In this study, we have demonstrated that therapeutic neovascularization using human umbilical cord blood-derived EPCs reversed diabetic neuropathy. EPCs were isolated and expanded on day 7 of culture from cord blood mononuclear cells. Unilateral intramuscular injection of EPCs into hindlimb skeletal muscles significantly ameliorated impaired sciatic motor nerve conduction velocity and sciatic nerve blood flow in the EPC-injected side of streptozotocin-induced diabetic nude rats compared with the saline-injected side of diabetic nude rats. Histological study revealed an increased number of microvessels in hindlimb skeletal muscles in the EPC-injected side of diabetic rats. These findings suggest that transplantation of EPCs from cord blood may be a useful treatment for diabetic neuropathy.

Animals↗
PubMed2005

[Case of thrombotic thrombocytopenic purpura with a positive Coomb test].

We report a case of thrombotic thrombocytopenic purpura (TTP) with a positive Coombs' test. A 59-year-old female was admitted to our hospital in February, 1997 with symptoms of heart failure. Ultrasound cardiography showed moderate pericardiac effusion and she was diagnosed as having pericarditis. After admission she had anorexia and her urine volume was reduced. Laboratory tests showed anemia and thrombocytopenia. Her Coombs' test result was positive. Her renal function gradually worsened and her conscious level was reduced. We diagnosed her as TTP and judged that she needed hemodialysis. We performed plasma exchange and started steroid therapy. The renal biopsy was compatible with TTP. After treatment, her level of consciousness improved, but her renal function did not improve. On the 51st hospital day she fell into acute respiratory distress syndrome (ARDS) and entered ICU. We considered ARDS caused by infection and continued treatment, but she died of shock and lactate acidosis. Activity of von Willebrand factor-cleaving protease in our case was 15% before the first PE, and 25 % just before death. A case of TTP without collagen disease usually shows a negative Coombs' test result. We think that this was a rare case in which autoimmune hemolytic anemia was supervened with TTP.

Acidosis, Lactic↗
PubMed2005

[Revised criteria for the early diagnosis of diabetic nephropathy].

The Diabetic Nephropathy Committee recommends the use of revised criteria for the early diagnosis of diabetic nephropathy in Japan. The new criteria are as follows: 1) Urinary albumin should be determined by immunoassay using a morning spot urine sample in diabetic patients without proteinuria or with dipstick-positive(+ 1) proteinuria. 2) A urinary albumin-to-creatinine ratio ranging from 30 to 299 mg/ gCr in 2 or more of 3 specimens may be diagnosed as microalbuminuria. 3) Two alternatives, i.e. the urinary albumin excretion rate of 30-299 mg/24hr in 24hr urine collection or 20-199 microg/min in timed urine collection can be used to detect microalbuminuria. 4) Renal hypertrophy and elevated urinary type IV collagen may indicate the existence of diabetic renal disease. 5) Microalbuminuria originating in non-diabetic diseases should be excluded.

Albuminuria↗
PubMed2004

Expression of CD46 in developing rat spermatozoa: ultrastructural localization and utility as a marker of the various stages of the seminiferous tubuli.

Identification of the various stages of the seminal tubule epithelium that are important in spermatogenesis in humans and rodents requires considerable expertise for analysis of ultrastructural appearance under light microscopy. Few good stage-specific markers have been reported to facilitate the process. We recently described characterization of the expression of CD46 (membrane cofactor protein) in the rat using a novel monoclonal antibody. Expression of CD46 was restricted to spermatozoa and their immediate precursors in the testis. In the present study, we used a combination of morphological analyses, known acrosome markers, actin staining, direct nuclear staining, and staining for CD46 to delineate precisely the subcellular location of CD46. Staining of CD46 colocalized with known acrosome markers in late spermatids and mature spermatozoa and was confirmed by electron microscopy to be acrosome-restricted. Expression was first detected in step 7 spermatids, whereas known markers were not expressed until step 9. The CD46 staining pattern differed through spermatid development, and distinct patterns of staining could be identified that, when combined with 4'-6-diamino-2-phenylindole-2HCl nuclear staining, enabled the accurate staging of the seminiferous tubule epithelium in different profiles. This detailed description of the spatiotemporal expression patterns of CD46 provides a valuable tool for analysis of spermatogenesis in the rat. Furthermore, this information will aid ongoing studies regarding the roles of CD46 in acrosome-related spermatozoal functions.

Acrosome↗
PubMed2004

Midkine expression in rat spinal motor neurons following sciatic nerve injury.

Midkine (MK), a heparin-binding growth factor, is produced in the developing and damaged nervous system. However, the role of MK in peripheral nerve injury has not been clarified. Here, we investigated MK expression in lumbar spinal motor neurons after rat sciatic nerve injury by immunohistochemical, in situ hybridization, and Western blot analyses. The rat sciatic nerve showed complete degeneration after local freezing. Numerous regenerated myelinated and thin nerve fibers were observed 3 weeks after injury. Intense MK immunoreactivity was detected in the ipsilateral spinal motor neurons of the anterior horn of the lumbar spinal cord after 1 day and in ipsilateral and contralateral spinal motor neurons from 4 days to 1 week after injury. It decreased after 2 weeks and again transiently increased in spinal motor neurons after 3 weeks. MK was found in the motor neurons and axon of the sciatic nerve. However, it was not detected in normal neurons and axon. In situ hybridization showed the expression of MK mRNA in lumbar spinal motor neurons of the anterior horn, but it was not present in Schwann cells or non-neuronal cells. Low-density lipoprotein receptor-related protein (LRP) immunoreactivity, a cell membrane receptor of MK, was observed in anterior horn motor neurons, but receptor-type protein tyrosine phosphatase zeta (PTPzeta) immunoreactivity as a signaling receptor complex of MK was not observed. LRP and PTPzeta immunoreactivities were observed in Schwann cells of the injured and uninjured sciatic nerve. Our findings suggest that MK is synthesized, released, and taken up in anterior horn motor neurons in an autocrine fashion with LRP. MK may have a role in degeneration and regeneration after peripheral nerve injury.

Animals↗
PubMed2004

A small interfering RNA targeting vascular endothelial growth factor as cancer therapeutics.

Vascular endothelial growth factor (VEGF) plays a critical role during normal embryonic angiogenesis and also in the pathological angiogenesis that occurs in a number of diseases, including cancer. We developed a novel VEGF blockade system using RNA interference. The small interfering RNA (siRNA) targeting human VEGF almost completely inhibited the secretion of VEGF in a human prostate cancer cell line, PC-3, whereas the control scramble siRNA showed no effects. The VEGF siRNA with atelocollagen dramatically suppressed tumor angiogenesis and tumor growth in a PC-3 s.c. xenograft model. Atelocollagen provided a beneficial delivering means by which stabilization and efficient transfection of the siRNA injected into the tumors were achieved.

Animals↗