PubMed Health⌕ Search

Biomedical subjects

Taro Matsumoto

Publications and source records attributed to Taro Matsumoto.

At least 19 recordsLinked to original sources
PubMed2006

Effects of G-CSF on cardiac remodeling and arterial hyperplasia in rats.

Although granulocyte colony-stimulating factor (G-CSF) has been shown to prevent cardiac remodeling after acute myocardial infarction, the mechanism and safety of G-CSF treatment acute myocardial infarction remain controversial. The purpose of the present study was to investigate in a rat model the mechanisms underlying the beneficial effect of G-CSF in acute myocardial infarction and to determine whether G-CSF treatment aggravates vascular remodeling of injured artery after acute myocardial infarction. Sprague-Dawley rats received transplanted bone marrow cells from green fluorescent protein (GFP) transgenic rats. Acute myocardial infarction was induced by ligation of the left coronary artery. After 24 h, the right carotid artery was injured with a balloon catheter. G-CSF (100 microg/kg/day) or saline was injected subcutaneously for 5 consecutive days after induction of acute myocardial infarction. G-CSF treatment significantly improved left ventricle function and reduced infarct size in rats with acute myocardial infarction. Expression of mRNA for the angiogenic cytokines was significantly higher in the infarction border area in the G-CSF group than in the control group. The surviving cardiomyocytes in infarction area were more in the G-CSF group. GFP-positive cells were gathered in the infarction border area in both groups; G-CSF did not increase cardiac homing of GFP-positive bone marrow cells in contrast to control group. Most GFP-positive cells were CD68-positive (macrophages). It was difficult to find bone marrow-derived cardiomyocytes in the infarcted area. G-CSF treatment inhibited neointima formation and increased reendothelialization of the injured artery. GFP-positive cells were identified most in the adventitia of the injured artery. A few cells in the neointima and reendothelialization were GFP positive. In conclusion, administration of G-CSF appears to be effective for treatment of left ventricular remodeling after acute myocardial infarction and does not aggravate vascular remodeling. The effect of G-CSF on cardiac and vascular remodeling may occur mainly through a direct action on the heart and arteries.

Actins↗
PubMed2006

Signal transduction via vascular endothelial growth factor (VEGF) receptors and their roles in atherogenesis.

Vascular endothelial growth factor (VEGF)-A plays a critical role in vascular development and angiogenesis through its binding and activation of VEGF receptor-2 (VEGFR-2). The binding of VEGF-A to VEGFR-2 causes receptor dimerization, kinase activation and autophosphorylation of specific tyrosine residues within the dimeric complex. Tyrosine(Y)951 in the kinase-insert domain, Y1054 and Y1059 in the kinase domain and Y1175 and Y1214 in the C-terminal tail have been shown to serve as autophosphorylation sites. Phosphorylated Y1175 creates a binding site for phospholipase Cgamma1 (PLC-gamma1) and Shb. Activation of PLC-gamma1 and Shb regulates VEGF-A-dependent cell proliferation and cell migration, respectively. Phosphorylated Y951 binds and mediates tyrosine phosphorylation of the T-cell-specific adaptor protein (TSAd), which is expressed in endothelial cells. Y951-mediated coupling of VEGFR-2 and TSAd is critical for VEGF-A-induced cell migration and actin reorganization, and for pathological angiogenesis. These phosphorylation sites may be useful targets for the development of anti-angiogenic therapies to treat atherosclerosis and cancer.

Atherosclerosis↗
PubMed2006

[Localized amyloidosis of the ureter: a case report].

A 46-year-old female was referred to our hospital with a complaint of left flank pain. Ultrasongraphy and computed tomography demonstrated a left hydronephroureter due to stenosis with a ureteral mass in the left lower ureter. Retrograde pyelography revealed severe stricture of left lower ureter and brushing cytology showed papanicolaou class III. Ureteral tumor was suspected and left nephroureterectomy with partial cystectomy was performed. Histopathological diagnosis was amyloidosis of the left ureter. There was no evidence of secondary or systemic amyloidosis. Finally, we diagnosed her with localized amyloidosis of the left ureter. Localized amyloidosis of the ureter is a relatively rare condition, and this is the 55th case reported in the Japanese literature.

Amyloidosis↗
PubMed2006

[Clinical evaluation of urinary NMP22 (nuclear matrix protein 22) bladder chek in the detection of patients with bladder cancer].

The clinical usefulness of the nuclear matrix protein 22 (NMP22) Bladder Chek test as a novel urine marker in the detection of patients with bladder cancer was evaluated in comparison with the urinary NMP22 enzyme-linked immunosorbent assay (ELISA) and urinary cytology. A total of 40 patients with pathologically proven bladder cancer voided urine specimen before treatment. The urine samples were divided for NMP22 Bladder Chek test, NMP22 ELISA, and urinary cytology. In the 40 patients with bladder cancer, the overall positive rate was 62.5% for the NMP22 Bladder Chek test, 55% for the NMP22 ELISA test, and 27.5% for urine cytology. There was a significant difference between NMP22 Bladder Chek, NMP22 ELISA and cytology. The positive rate with the NMP22 Bladder Chek and NMP22 ELISA was higher in the patients with high grade and large-size (1 cm < or =) tumor. In 40 patients presenting with microhematuria without urothelial cancer, the false positive rate 12.5, 10, and 0% for NMP22 Bladder Chek, NMP22 ELISA, and urinary cytology. No significant difference was found with the test. In conclusion, the urine NMP22 Bladder Chek test provided a higher positive rate than the NMP22 ELISA test and urinary cytology. Therefore, the NMP22 Bladder Chek test may be clinically more useful as a tumor marker for the diagnosis of bladder cancer.

Adult↗
PubMed2006

[Inflammatory pseudotumor of the urinary bladder: a case report].

A 65-year-old female was referred to our hospital with a complaint of urinary retention and macrohematuria. Ultrasongraphy, computed tomography, magnetic resonance imaging and cystoscopy revealed a 2 x 2 cm broad-based nonpapillary bladder tumor localized in the anterior wall of the urinary bladder. The clinical diagnosis was an invasive bladder tumor and transurethral resection of bladder tumor carried out for pathological investigation. Finally, we diagnosed it as inflammatory pseudotumor of urinary bladder. No local recurrence was seen 12 months after surgery. Inflammatory pseudotumor of urinary bladder is a relatively rare condition, and this is the 52nd case reported in the Japanese literature.

Aged↗
PubMed2006

[Early effect of non-surgical treatment using betamethasone valerate ointment for phimosis in childhood].

We evaluated the early efficacy of non-surgical treatment using 0.07% betamethasone valerate ointment on, 34 boys with phimosis between January 2001 and June 2005. Patients were treated with 0.07% betamethasone valerate ointment applied to the distal aspect of the prepuce every other day for 2-6 weeks. During the treatment period, patients were instructed to retract the foreskin to penis root without overstraining. The overall success rate was 94.1% and therapeutic effects were observed in 58.8% of the patients in two weeks. There were no medical side effects. Treatment using betamethasone valerate ointment is very effective, easy and safe. We recommend this treatment for patients with phimosis and/or those with recurring balanoposthitis.

Anti-Inflammatory Agents↗
PubMed2006

[A clinical study of renal pelvic and ureteral cancer].

We investigated the clinicopathological features of 52 patients with transitional cell carcinoma of renal pelvic and/or ureter who underwent surgical treatment at Tokyo Medical University Hachioji Medical Center from April, 1992 to June, 2005. The patitents consisted of 38 males and 14 females, ranging from 29 to 86 years old with a median age of 68 years old. The mean follow-up period was 39 months. Pathologicaly, 32 cases were less than pT2 and 20 cases were pT3. Findings of lymphatic and venous invasion were present in 10 and 8 cases, respectively. The infiltration pattern (INF) of gamma was observed in 9 cases. The overall cause-specific survival rate was 95.8% at 1 year, 87.7% at 3 years and 80.6% at 5 years, respectively. According to univariate analysis, the high stage of tumor, the presence of lymphatic and/or venous invasion, the inclusion of infiltration pattern of gamma and positive reginonal lymph nodes indicated a significantly poor prognosis. On the other hand, multivariate analysis using Cox proportional hazards regression revealed the presence of infiltration pattern of gamma as the most significant predictor of survival.

Adult↗
PubMed2005

Proteomic analysis of vascular endothelial growth factor-induced endothelial cell differentiation reveals a role for chloride intracellular channel 4 (CLIC4) in tubular morphogenesis.

Formation of new vessels from pre-existing capillaries demands extensive reprogramming of endothelial cells through transcriptional and post-transcriptional events. We show that 120 protein spots in a two-dimensional isoelectric focusing/electrophoretic analysis were affected during vascular endothelial growth factor-A-induced endothelial cell tubular morphogenesis in vitro, as a result of changes in charge or expression level of the corresponding proteins. For about 22% of the spots, the protein products could be identified, of which several previously have been implicated in cytoskeletal reorganization and angiogenesis. One such protein was heat shock protein 27, a chaperone involved in beta-actin rearrangement that was identified as regulated in degree of serine phosphorylation. We also identified regulation of chloride intracellular channel 4 (CLIC4), the expression of which decreased during tubular morphogenesis. CLIC4 was expressed at high levels in resting vessels, whereas expression was modulated during pathological angiogenesis such as in tumor vessels. The subcellular localization of CLIC4 in endothelial cells was dependent on whether cells were engaged in proliferation or tube formation. Antisense- and small interfering RNA-mediated suppression of CLIC4 expression led to arrest in tubular morphogenesis. Our data implicate CLIC4 in formation of a vessel lumen.

Base Sequence↗
PubMed2005

VEGF receptor-2 Y951 signaling and a role for the adapter molecule TSAd in tumor angiogenesis.

Vascular endothelial growth factor receptor-2 (VEGFR-2) activation by VEGF-A is essential in vasculogenesis and angiogenesis. We have generated a pan-phosphorylation site map of VEGFR-2 and identified one major tyrosine phosphorylation site in the kinase insert (Y951), in addition to two major sites in the C-terminal tail (Y1175 and Y1214). In developing vessels, phosphorylation of Y1175 and Y1214 was detected in all VEGFR-2-expressing endothelial cells, whereas phosphorylation of Y951 was identified in a subset of vessels. Phosphorylated Y951 bound the T-cell-specific adapter (TSAd), which was expressed in tumor vessels. Mutation of Y951 to F and introduction of phosphorylated Y951 peptide or TSAd siRNA into endothelial cells blocked VEGF-A-induced actin stress fibers and migration, but not mitogenesis. Tumor vascularization and growth was reduced in TSAd-deficient mice, indicating a critical role of Y951-TSAd signaling in pathological angiogenesis.

Actins↗
PubMed2005

Body distribution of trace elements in black-tailed gulls from Rishiri Island, Japan: age-dependent accumulation and transfer to feathers and eggs.

Body distribution and maternal transfer of 18 trace elements (V, Cr, Mn, Co, Cu, Zn, Se, Rb, Sr, Mo, Ag, Cd, Sb, Cs, Ba, Hg, Tl, and Pb) to eggs were examined in black-tailed gulls (Larus crassirostris), which were culled in Rishiri Island, Hokkaido Prefecture, Japan. Manganese, Cu, Rb, Mo, and Cd showed the highest levels in liver and kidney, Ag, Sb, and Hg in feather, and V, Sr, and Pb in bone. Maternal transfer rates of trace elements ranged from 0.8% (Cd) to as much as 65% (Tl) of maternal body burden. Large amounts of Sr, Ba, and Tl were transferred to the eggs, though maternal transfer rates of V, Cd, Hg, and Pb were substantially low. It also was observed that Rb, Sr, Cd, Cs, and Ba hardly were excreted into feathers. Concentrations of Co in liver, Ba in liver and kidney, and Mo in liver increased significantly with age, whereas Se in bone and kidney, Hg in kidney, and Cr in feather decreased with age in the known-aged black-tailed gulls (2-20 years old). It also was suggested that feathers might be useful to estimate contamination status of trace elements in birds, especially for Hg on a population basis, although the utility is limited on an individual basis for the black-tailed gulls. To our knowledge, this is the first report on the maternal transfer rate of multielements and also on the usefulness of feathers to estimate contamination status of Hg in birds on a population basis.

Animals↗
PubMed2004

The adaptor protein shb binds to tyrosine 1175 in vascular endothelial growth factor (VEGF) receptor-2 and regulates VEGF-dependent cellular migration.

Previous studies have shown that the adaptor protein Shb is involved in receptor tyrosine kinase signaling. In this study, we demonstrate that Shb is phosphorylated in an Src-dependent manner upon vascular endothelial growth factor (VEGF) stimulation using porcine aortic endothelial cells expressing the human VEGF receptor 2 (VEGFR-2) (KDR). In co-immunoprecipitation experiments, we could detect an interaction between Shb and the VEGFR-2 in human telomerase-immortalized microvascular endothelial cells. Furthermore, in a glutathione S-transferase pull-down assay, the Src homology 2 domain of Shb was shown to interact with phosphorylated tyrosine 1175 in the C-terminal tail of VEGFR-2. VEGF-induced Shb phosphorylation was lost in porcine aortic endothelial cells expressing a chimeric murine VEGFR-2 (Flk-1) with a mutation at the corresponding position. Shb expression was specifically decreased by 80%, in a transient manner, by using the short interfering RNA technique. Reduced Shb expression led to a loss of stimulation of phosphatidylinositol 3-kinase, phosphorylation of focal adhesion kinase at tyrosine 576, the generation of focal adhesions, and stress fiber formation in response to VEGF. Furthermore, we show that VEGF-induced migration is inhibited in Shb short interfering RNA-treated cells. Our data demonstrate that Shb is important for VEGF signaling in endothelial cells. This is achieved by Shb binding to tyrosine 1175 in the VEGFR-2, which regulates VEGF-induced formation of focal adhesions and cell migration, of which the latter occurs in a phosphatidylinositol 3-kinase-dependent manner.

Actins↗
PubMed2004

Development of angiogenic cell and gene therapy by transplantation of umbilical cord blood with vascular endothelial growth factor gene.

Endothelial progenitor cells (EPCs) are present in the mononuclear cells (MNCs) of umbilical cord blood and peripheral blood. To establish the efficiency of angiogenic cell and gene therapies, we transfected the human vascular endothelial growth factor (hVEGF) gene into cord blood MNCs to enhance endothelialization. MNCs from cord blood and peripheral blood were isolated and transfected with pCR3 expressing hVEGF165 or GFP by the Hemagglutinating Virus of Japan (HVJ)-envelope and the cells were cultured in endothelium basal medium-2. The number of attached cells from cord blood was higher than that from peripheral blood. Attached cells expressed Flk-1, VE-cadherin, PECAM-1, CD34, and Tie-2. The increase in the number of attached cells was transient with the transfection of vascular endothelial growth factor (VEGF) gene early in the experimental period. Flt-1 mRNA was not expressed early in the culture period, but was expressed at 2 weeks after separation. VEGF gene transfer into MNCs at 12 days after separation, i.e., when Flt-1 mRNA was expressed continuously, increased the number of attached cells. We evaluated the effects of the transplantation of cord blood MNCs expressing the hVEGF gene on regional blood flow in an ischemic area in a rat model of chronic hindlimb ischemia. Blood flow was significantly improved in nude rats that received transplanted control MNCs. Transplantation of cord blood MNCs transfected with the hVEGF gene yielded greater improvements in blood flow. These results indicate that the hVEGF gene enhances endothelialization of EPCs, and that the transplantation of cord blood MNCs transfected with the VEGF gene may be feasible for the treatment of ischemic diseases as a type of angiogenic cell and gene therapy.

Animals↗
PubMed2004

[Atherosclerotic regression in the aortas of elderly. (4). Expression of peroxisome proliferator-activated receptors with references of centrally depressed atherosclerotic plaque].

Peroxisome proliferator-activated receptors (PPARs) play an important role in vascular events during progression of atherosclerosis, associated with lipid metabolism, inflammatory response and others. To clarify relationships between the expression of PPARs subtypes and regression, we studied mRNA expression of PPARs subtypes with reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry, especially in centrally depressed atherosclerotic plaques (depressed plaque) in the aortas of elderly patients, and proposed morphological feature of atherosclerotic regression. Samples were separated from the depressed plaque, atheromatous plaque, and diffuse intimal thickening (DIT) in the aortas of elderly patients at autopsy and they were analyzed for RT-PCR. The depressed plaques obtained were divided into two parts: depressed area and surrounding elevated area. Total RNA was prepared, using the TRIzol Reagent, and was reverse transcribed using random hexamer primers and Thermoscript kit for RT-PCR. Immunohistochemical analysis was processed for mouse anti-PPAR gamma antibody, detected by the ABC method. 1) Decreased foam cells were found in the depressed area than in the surrounding elevated area of the depressed plaque. These foam cells were immunohistochemically positive for HAM56 and strong reactivities for PPAR gamma were found in the nuclei of macrophage-derived foam cells. PPAR gamma was also detected in the nuclei of endothelial cells and smooth muscle cells. 2) Expressions of PPAR alpha and PPAR gamma were found in the depressed plaques with RT-PCR. These expressions were found both in the depressed area and the surrounding elevated area without significant differences. 3) PPAR gamma mRNA expression both in the depressed area and the surrounding elevated area, was greater than in DIT, and was less than in the atheromatous plaque. 4) Expression of PPAR gamma mRNA was intense and increased in the surrounding elevated area than in the depressed area. 5) A significant increase of PPAR gamma expression was found in the atheromatous plaque than in the DIT. 6) There was no significant difference of PPAR alpha mRNA expression between the depressed area and the surrounding elevated area. The depressed plaque has been considered to be a morphological characteristic of regression in recent studies. Expression of mRNA for PPARs was detected in the depressed plaque as well as the atheromatous plaque, furthermore, there were different expressions and intensity of PPARs between the depressed area and the surrounding elevated area of the depressed plaque. These findings suggest that the expression of PPARs may be involved not only in the progression of atherosclerosis but also in regression.

Adult↗
PubMed2003

Endostatin action and intracellular signaling: beta-catenin as a potential target?

Endostatin, the C-terminal part of collagen XVIII, has been shown to inhibit blood vessel formation in different pathological conditions characterized by increased angiogenesis, such as growing tumors. Subcutaneous injection of endostatin in tumor-bearing mice leads to decreased tumor growth, and even in some cases, cure of tumor disease. Endostatin has been tested in a clinical phase I study and shown not to be toxic. Whether the finding in mice that endostatin treatment does not result in development of resistance will hold true in humans is too early to tell. Endostatin binds to a specific motif in heparan sulfate, which may serve a co-receptor function. The structure of a potential primary receptor is not known. The mechanism of action of endostatin in inhibition of angiogenesis and thereby, inhibition of tumor growth, involves apoptosis of tumor cells. The most consistent effect of endostatin on endothelial cells in vitro is inhibition of endothelial cell migration, which may be due to disturbed cell-matrix interactions. An interesting candidate for transducing endostatin's effect on apoptosis and cell migration is beta-catenin, an intracellular protein which participates both in cell adhesion and in transcriptional regulation.

Angiogenesis Inhibitors↗
PubMed2003

VEGF-receptor signal transduction.

The vascular endothelial growth factor (VEGF) family of ligands and receptors has been the focus of attention in vascular biology for more than a decade. There is now a consensus that the VEGFs are crucial for vascular development and neovascularization in physiological and pathological processes in both embryo and adult. This has facilitated a rapid transition to their use in clinical applications, for example, administration of VEGF ligands to enhance vascularization of ischaemic tissues and, conversely, inhibitors of VEGF-receptor function in anti-angiogenic therapy. More recent data indicate essential roles for the VEGFs in haematopoietic cell function and in lymphangiogenesis.

Animals↗
PubMed2003

Paraoxonase1 polymorphism Leu-Met55 is associated with cerebral infarction in Japanese population.

BACKGROUND: Paraoxonase1 (PON1) is HDL-associated ester hydrolase which has been shown to prevent LDL and HDL oxidation in vitro. PON1-coding region has two common polymorphisms (M/L55 and A/B192) that influence PON activity. We examined whether these polymorphisms relates with the incidence of cerebral infarction (CI) which is one of the major atherosclerotic disease in Japan. MATERIAL/METHODS: The study population was comprised of 112 unrelated Japanese CI patients and 106 healthy Japanese individuals. The PON1 genotypes were determined by PCR and digestion by specific restriction enzymes. RESULTS: PON1-192 polymorphism revealed no significant difference of genotype and allelic distribution in CI patients and controls. Frequency of L/M alleles in PON1-55 polymorphism (0.88, 0.12, respectively) was different from previously reported frequencies in Caucasians. Comparison of allelic distribution of the PON1-55 polymorphism showed a significant increase of the M allele in CI subjects compared with control subjects. All three subjects with the MM genotype were in the CI group. Of subjects with an AA genotype, the frequencies of the MM and LM genotypes were significantly higher and that of the LL genotype was significantly lower in the CI group compared with the control group. Frequency of the M allele in the CI group was significantly higher in subjects who had the AA genotype. CONCLUSIONS: These findings suggest that the enzyme might be involved in the development of atherosclerosis of cerebral arteries. Moreover, this finding might indicates that the genetic markers in Japanese linked to distinct genetic event from Caucasians.

Adult↗