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Biomedical subjects

I Katoh

Publications and source records attributed to I Katoh.

At least 19 recordsLinked to original sources
PubMed1999

Induction of manganese-superoxide dismutase in MRC-5 cells persistently infected with an alphavirus, sindbis.

Sindbis virus (SV), a single-stranded positive-sense RNA virus, multiplies in a variety of cells and causes various outcomes of infection. As we described acute infection of SV induces stress response of small heat shock protein HSP27 and activation of mitogen-activated protein kinase (MAP) signaling pathway (Nakatsue, T., et al., Biochem. Biophys. Res. Commun. 253, 59-64, 1998). In contrast to lytic infection in Vero cells, MRC-5 cells, a human fetus lung cell line, resulted in persistent infection by SV. Here we investigated a cellular factor involved in persistent infection of MRC-5 cells infected with SV. Partial sequence analysis of a 25 kilodalton (kDa) protein, accumulated in large amounts in the cells, showed that manganese-superoxide dismutase (Mn-SOD) was induced during the infections. When Mn-SOD was overexpressed in Vero cells, 20% of the cells survived more than one month, in contrast with the death of 99% of the vehicle-transfected Vero cells at 48 h after infection with SV. These data strongly suggest that a cellular factor which regulates the oxidative pathway modulates the outcome of SV infection.

Amino Acid Sequence↗
PubMed1999

Surgical management of infants with mitral valve stenosis or atresia without diminutive ascending aorta.

The surgical strategy in infants with mitral valve stenosis or atresia without diminutive ascending aorta remains to be established, including the potential for biventricular repair as a definitive operation. Our surgical experience of six infants with mitral valve stenosis (4 patients) or atresia (2 patients) without diminutive ascending aorta was evaluated based on three important factors: left ventricular volume; the nature of the systemic outflow obstruction; and the type of mitral valve anomaly. Two patients with systemic outflow tract diameter less than 65% of normal underwent systemic outflow tract reconstruction, and the other patients with outflow tract diameter more than 68% of normal were able to maintain systemic circulation without repair. Only one patient with mitral valve stenosis without left ventricular outflow tract obstruction underwent a successful open mitral valvotomy as a biventricular repair after first-stage palliation. The left ventricle of the other patients did not grow after first-stage palliation. Due to progressive subaortic narrowing, pulmonary artery banding should be avoided in patients with mitral atresia due to absent atrioventricular connection who are future Fontan candidates. Most patients with this lesion can be expected to become candidates for safe Fontan-type repair.

Aorta↗
PubMed1998

Acute infection of Sindbis virus induces phosphorylation and intracellular translocation of small heat shock protein HSP27 and activation of p38 MAP kinase signaling pathway.

In general, viral infection is supposed to induce stress responses in the host cell. However, very few detailed observations about virus-induced stress responses have been reported. Here we investigated specific stress responses in Vero cells infected with Sindbis virus (SV), a single-stranded RNA virus, acute infection with which is known to cause apoptotic cell death in the host cells. Prior to the onset of apoptosis, p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinases (JNKs) were activated. Subsequently, a 27-kDa heat shock protein (HSP27) became phosphorylated, and intracellular distribution of HSP27 was changed from the cytoplasm to the perinuclear region. These results indicate that the cellular signaling cascades activated by pro-inflammatory cytokines and environmental stresses are also activated as a result of lytic infection with SV. These responses may contribute to the delayed onset of apoptosis in the host cells and the facilitation of viral replication.

Animals↗
PubMed1998

Effect of angiotensin II on Ca2+ efflux from freshly isolated adult rat cardiomyocytes: possible involvement of Na+/Ca2+ exchanger.

In the present study, we examined the effect of angiotensin II on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Angiotensin II stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner, at least in pharmacological doses of 10(-8) M to 10(-5) M. The 45Ca2+ efflux was inhibited by the type 1 angiotensin II receptor antagonist losartan, but not by the type 2 antagonist PD 123319. Angiotensin II also induced an increase in cytosolic free calcium ([Ca2+]i) and inositol trisphosphate formation within the cardiomyocytes. Angiotensin II-induced 45Ca2+ efflux and the increase in [Ca2+]i were both inhibited by thapsigargin, a specific inhibitor of the sarcoplasmic reticulum Ca2+ pump. The 45Ca2+ efflux was not affected by removal of the extracellular Ca2+ but was dependent on the presence of extracellular Na+. In addition, angiotensin II caused 22Na+ influx into the cells. These results indicate that angiotensin II stimulates Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on the plasma membrane type 1 angiotensin II receptors. Angiotensin II-induced increase in [Ca2+]i may cause an activation of Na+/Ca2+ exchange which finally results in the stimulation of 45Ca2+ efflux from the cells. Since it is reported that Na+/Ca2+ exchange is important in calcium homeostasis within the cells, angiotensin II may play some role in the reduction of intracellular Ca2+ from isolated adult rat cardiomyocytes.

Angiotensin II↗
PubMed1998

Changes in plasma free and sulfoconjugated dopamine in patients with congenital heart disease who underwent cardiac operation.

It has been suggested that plasma sulfoconjugated dopamine (DA) may serve as a source or reservoir for free DA in plasma. Moreover, it has also been reported that the plasma levels of conjugated DA may be used as an index predicting heart failure in patients with heart disease. Therefore, in the present study, we have measured the plasma levels of free and sulfoconjugated DA in patients with congenital heart disease who underwent total corrective operations. The patients were divided into two groups with (6 patients with tetralogy of Fallot, TOF) or without (5 patients with ventricular septal defect without pulmonary hypertension, VSD) cyanosis (mean age of 2.11 years). Blood samples were collected before and after operation from the patients, and plasma free and sulfoconjugated DA levels were measured using high performance liquid chromatography. Preoperative levels of free DA in patients in both groups were higher than the level in age matched control subjects. The plasma level of conjugated DA in TOF was higher than that in the controls and was the highest in VSD before operation. DA infusion early after operation caused a rise in plasma free and conjugated DA, however, the levels of increased free DA were lower in the VSD than in the TOF group. After discontinuing DA infusion, the plasma levels of free DA remained higher, while those of conjugated DA decreased to a level lower than the preoperative values in both groups. As the plasma levels of free and sulfoconjugated DA vary with hemodynamics, it was assumed that the difference in the plasma sulfoconjugated DA level between the groups before operation was due to the influence of pulminary blood flow on catecholamine homeostasis. Since the decrease in conjugated DA has been postulated to be an index of sustained heart failure, it is conceivable that it takes a long time for patients who underwent cardiac operations in infancy to recover from heart failure.

Child, Preschool↗
PubMed1998

[A case of reoperation 24 years after repair of absent pulmonary valve syndrome with anomalous origin of the left pulmonary artery].

We experienced a case of a 38-year-old woman with a persistent cough, 24 years after repair of absent pulmonary valve syndrome with anomalous origin of the left pulmonary artery. The right pulmonary artery was massively dilated, thus it caused the compression of the bronchi, which was thought to result in her respiratory symptom. This dilatation of the right pulmonary artery seemed to have progressed because of the following two reasons. The first is the pulmonary hypertension caused by the late reconstruction of the left pulmonary artery. The second is residual pulmonary stenosis and regurgitation after the initial operation without a pulmonary valve insertion. We performed a reoperation consisting of reconstruction of the right ventricular outflow tract using a valved conduit and plication of the right pulmonary artery. Her postoperative course has been without any complications and satisfactory for the past 2 years.

Adult↗
PubMed1998

Extracellulary administered lysophosphatidylcholine causes Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

It has previously been reported that ischemia and reperfusion of the heart cause accumulation of lysophosphatidylcholine (LPC) within the myocardium. While it is known that LPC causes the transient increase of intracellular free Ca2+ concentration ([Ca2+]i) during contraction of cardiac cells, little is known about the mechanism for decreasing [Ca2+]i in cardiomyocytes during LPC accumulation. Since cumulative elevation in [Ca2+]i leads to irreversible injury to cardiomyocytes, elevated [Ca2+]i must be restored to an unstimulated level to maintain cell functions. In the present study, we therefore examined the effect of LPC on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. LPC stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-7)M-10(-5)M). Other lysophospholipids, which are generated from phospholipids of the cell membrane, failed to induce 45Ca2+ efflux from the cells. Dilazep and K-7259, which are known to inhibit the increase in [Ca2+]i caused by LPC, likewise reduced 45Ca2+ efflux caused by LPC addition. Furthermore, the LPC-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. On the other hand, inhibitors of Na+/Ca2+ exchange, amiloride and 5-(N,N-dimethyl)-amiloride, inhibited LPC induced 45Ca2+ efflux. These results suggest that LPC stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange on the plasma membrane of the cells.

Adenosine Triphosphate↗
PubMed1998

Cloning and functional analysis of human p51, which structurally and functionally resembles p53.

The p53 tumor suppressor gene, which is induced by DNA damage and/or stress stimuli, causes cells to undergo G1-arrest or apoptotic death; thus it plays an essential role in human carcinogenesis. We have searched for p53-related genes by using degenerate PCR, and have identified two cDNA fragments similar to but distinct from p53: one previously reported, p73, and the other new. We cloned two major splicing variants of the latter gene and named these p51A and p51B (a human homologue of rat Ket). The p51A gene encodes a 448-amino-acid protein with a molecular weight of 50.9 kDa; and p51B, a 641-amino-acid protein with a molecular weight of 71.9 kDa. In contrast with the ubiquitous expression of p53, expression of p51 mRNA was found in a limited number of tissues, including skeletal muscle, placenta, mammary gland, prostate, trachea, thymus, salivary gland, uterus, heart and lung. In p53-deficient cells, p51A induced growth-suppression and apoptosis, and upregulated p21waf-1 through p53 regulatory elements. Mutations in p51 were found in some human epidermal tumors.

Alternative Splicing↗
PubMed1998

Effect of amiloride on ischaemia and reperfusion injury in isolated, perfused rat hearts.

The effect of amiloride, a potent inhibitor of Na+/H+ exchange, on ischaemic reperfused rat hearts was studied in order to investigate whether Na+/H+ exchange or Na+/Ca2+ exchange is involved in ischaemia-reperfusion injury, When hearts were pre-ischaemically loaded with 100 microM amiloride, recovery of left ventricular developed pressure was significantly better than in control hearts, whereas recovery of heart rate at 30-min reperfusion was unaffected. Amiloride pretreatment also decreased creatine phosphokinase activity in the coronary effluent and completely abolished occurrence of ventricular arrhythmias during reperfusion. It also inhibited intracellular Na+ accumulation early in reperfusion (within 5 min), whereas in the late stage (from 5 to 30 min), Ca2+ overload was inhibited. The findings suggest that Na+/H+ exchange participates mainly in the early stage of reperfusion injury and the Na+/Ca2+ exchange system, secondary to Na+/H+ exchange, in the late stage. The reduction in post-ischaemic cardiac dysfunction induced by amiloride pretreatment may be attributable to inhibition of the resultant Ca2+ accumulation during reperfusion.

Amiloride↗
PubMed1997

Atrial natriuretic peptide stimulates Na+-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

In the present study, we examined the effect of atrial natriuretic peptide (ANP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Rat ANP(1-28) stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-8) M to 10(-6) M). The 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. In addition, rat ANP(1-28) caused 22Na+ influx into the cells. The 45Ca2+ efflux was also stimulated by C-type natriuretic peptide-22 (CNP-22), but not by rat brain natriuretic peptide-45 (BNP-45). It was also observed that both rat ANP(1-28) and CNP-22 stimulated guanosine 3',5'-cyclic monophosphate production within the cells. These results indicate that ANP stimulates Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through Na+/Ca2+ exchange, and that the stimulatory effect of ANP on Ca2+ efflux may be mediated via the natriuretic peptide receptor which has been shown to couple to guanylate cyclase. Since it is reported that Na+/Ca2+ exchange is important in calcium homeostasis within cells, ANP may play a role in the extrusion of intracellular Ca2+ from isolated adult rat cardiomyocytes.

Animals↗
PubMed1997

Neuropeptide Y as a stimulator of Na+ -dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

Several physiological stimuli cause a rise in intracellular Ca2+ concentration ([Ca2+]i) in cardiomyocytes. This increased [Ca2+]i must be restored to physiological resting level to ensure response to further stimuli. In the present study, we examined the effect of neuropeptide Y (NPY), which is secreted from certain adrenergic or nonadrenergic neurons, on Ca2+ efflux from freshly isolated, quiescent adult rat cardiomyocytes. The isolated cardiomyocytes were preloaded with 45CaCl2 for 1 h. Then, the fractional release of 45Ca2+ from the cells was measured. NPY stimulated the efflux of 45Ca2+ from isolated adult rat cardiomyocytes in a concentration-dependent manner (10(-8) M to 10(-6) M). NPY (10(-6) M)-induced Ca2+ efflux was 2.0 +/- 0.16% of the total cellular content. The 45Ca2+ efflux from the cells was also stimulated by Y1 receptor agonist, [Leu31, Pro34]NPY, but not by Y2 receptor agonist, NPY13-36. The effect of NPY was inhibited by a peptide NPY inhibitor, NPY18-36 and a non-peptide NPY inhibitor, benextramine to a similar extent. From these results, it is conceivable that the effect of NPY on Ca2+ efflux from cardiomyocytes is mediated through Y1 receptors. It was also observed that NPY caused a rise in [Ca2+]i to almost 150 nM. NPY-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, NPY caused a 22Na+ influx into the cells of about 1.6-fold over the basal value which was inhibited by amiloride and 5-(N,N-dimethyl)-amiloride, known Na+/Ca2+ exchange inhibitors. In addition, isoproterenol also caused 45Ca2+ efflux from the cells and which was enhanced by the addition of NPY. These results suggest that NPY stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane Y1 receptors with which NPY may couple during Na+/Ca2+ exchange.

Adenosine Triphosphatases↗
PubMed1997

Effect of docarpamine, a novel orally active dopamine prodrug, on the formation of free and sulfoconjugated dopamine in patients who underwent cardiac surgery.

To evaluate the clinical efficacy of orally active dopamine prodrug, docarpamine [N-(N-acetyl-L-methionyl)-O,O-bis (ethoxycarbonyl) dopamine], we examined its effect on the formation of free and sulfoconjugated dopamine in patients who underwent cardiac surgery. The preoperative values of free and sulfoconjugated dopamine in patients were 216 +/- 52 pg/ml and 4,930 +/- 820 pg/ml, respectively. The plasma level of free dopamine increased to 95.3 +/- 28.3 ng/ml by dopamine infusion after the operation and was sustained at a high level (87.7 +/- 26.5 ng/ml) by concomitant administration of docarpamine in spite of tapering of dopamine infusion. After stopping dopamine infusion, plasma level of free dopamine was 24.5 +/- 17.6 ng/ml maintained by oral administration of docarpamine alone. From these results, docarpamine may be a useful alternative to intravenous dopamine after cardiac surgery. Sulfoconjugated dopamine in plasma increased to 267 +/- 120 ng/ml after the start of dopamine infusion and increased further after oral docarpamine administration to 2,060 +/- 610 ng/ml. Since sulfoconjugated dopamine is thought to be a possible precursor of active free dopamine in plasma, orally administered docarpamine might be stored as a reserve pool for free dopamine in patients who undergo cardiac surgery.

Administration, Oral↗
PubMed1997

Extracellular adenosine 5'-triphosphate induces Ca2+ efflux from freshly isolated adult rat cardiomyocytes: possible involvement of Na+/Ca2+ exchange mechanism.

In the present study, we examined the effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. ATP at 1 mM caused a release of 3.6+/-0.08% of the total cellular content. The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate) (ATP-gamma s), alpha, beta-methylene-ATP and adenosine 5'-diphosphate (ADP), but not by adenosine 5'-monophosphate (AMP) or adenosine. The effect of ATP was inhibited by a known purinergic P2-receptor antagonist, but not by a P1-receptor antagonist. From these results, it is conceivable that the effect of ATP on Ca2+ efflux from cardiomyocytes is mediated through P2-purinoceptors. It was also observed that ATP caused a rise in [Ca2+]i to almost 200 nM. The ATP-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, ATP caused a 22Na+ influx into the cells of about 2.0-fold over the basal value. These result suggest that ATP stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane P2-purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine Triphosphate↗
PubMed1996

Angiotensin II as a stimulator of Na(+)-dependent Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

In cardiac tissues, angiotensin II causes inotropic and chronotropic effects on the heart. It is indicated that the mechanism of the inotropic effect of angiotensin II is attributed to an increase in cytosolic free calcium ([Ca2+]i) in cardiomyocytes. However, increased [Ca2+]i should be restored to a physiological level because cumulative elevation in [Ca2+]i leads to irreversible injury in cardiomyocytes. Whereas it is known that angiotensin II causes the increase in [Ca2+]i in cardiac cells, little is known about the mechanisms of decrease in [Ca2+]i in cardiomyocytes upon angiotensin II stimulation. In the present study, we examined the effect of angiotensin II on Ca2+ efflux from freshly isolated adult rat cardiomyocytes. Angiotensin II stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (10(-7)-10(-5) M). The 45Ca2+ efflux from the cells was inhibited by type 1 angiotensin II receptor inhibitor. The angiotensin II-stimulated 45Ca2+ efflux was not affected by deprivation of the extracellular Ca2+, but was dependent on the presence of extracellular Na+. These results indicate that angiotensin II stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on the plasma membrane type 1 angiotensin II receptors which may couple to Na+/Ca2+ exchange.

Angiotensin II↗
PubMed1996

Effect of extracellular adenosine 5'-triphosphate on Ca2+ efflux from freshly isolated adult rat cardiomyocytes.

The effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+ efflux from freshly isolated adult rat cardiomyocytes was examined. ATP stimulated the efflux of 45Ca2+ from the cells in a concentration-dependent manner (0.01-1 mM). The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate)(ATP-gammas) and alpha,beta-methylene-ATP and adenosine 5'-diphosphate, but not by adenosine 5'-monophosphate and adenosine. The ATP-stimulated 45Ca2+ efflux was not affected by deprivation of the extracellular Ca2+, but was dependent on the presence of extracellular Na+. These results indicate that ATP stimulates extracellular Na+-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on the plasma membrane P2 purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine↗
PubMed1996

Physiological significance of plasma sulfoconjugated dopamine in patients with hypertension--clinical and experimental studies.

Sulfoconjugated catecholamines, especially dopamine sulfate, have recently attracted much attention because of the possibility of their conversion to active free dopamine by tissue arylsulfatase. In the present study, we have measured the plasma levels of free and sulfoconjugated dopamine in patients with hypertension and have investigated the physiological significance of sulfoconjugation. Results showed that the plasma level of dopamine sulfate in patients with essential hypertension was higher than the level in control subjects, and was highest in patients with renal hypertension. However, the plasma level of free dopamine showed no significant difference between patients with hypertension and normal subjects. Moreover, after normalization of blood pressure in hypertensive patients with medication, the plasma levels of conjugated dopamine decreased to almost the control value. In the experimental study, dopamine sulfate inhibited angiotensin II-induced aldosterone release from bovine adrenal cortical cells to a similar extent as produced by free dopamine. From these results, we have concluded that plasma sulfoconjugated dopamine may regulate free dopamine in the plasma of patients with hypertension, and it may have some physiological effects on blood pressure regulation.

Adrenal Cortex↗
PubMed1996

[Surgical experience of two different types of unroofed coronary sinus].

We experienced two cases with uncommon unroofed coronary sinus. The first patient, a 55-year-old man, had a partially unroofed mid-portion of the coronary sinus. His symptoms and physical state were similar to that of atrial septal defect (ASD). Echocardiogram and angiogram revealed that the coronary sinus (CS) communicated with the left atrium (LA). We confirmed that CS had an enlarged orifice and lacked a part of its roof through the right atriotomy and the atrioseptotomy. We directly closed the defect between the LA and the CS. His postoperative course was satisfactory. The second patient, a 46-year-old man, showed mild cyanosis. He had a completely unroofed CS with left superior vena cava (LSVC), absent inferior vena cava (IVC) and hemiazygos continuity. The LSVC directly drained to the LA, and the CS was absent. A part of the posterior wall of the LA was like a groove which laid from the orifice of the LSVC to the coronary sinus ASD. The roof of this groove was covered with fibrous tissue, which was shaped like a network structure. We thought that this network was a residue of the septum between the CS and the LA. Thus we resected this structure, and reconstructed the roof by equine pericardial patch to drain the venous blood from the LSVC to the right atrium. Anomaly in the patient may be the transitional type between the completely unroofed CS and the partially unroofed CS.

Coronary Vessel Anomalies↗