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Rie Inoue

Publications and source records attributed to Rie Inoue.

8 recordsLinked to original sources
PubMed2006

Heterogeneity and tissue specificity of tropomyosin isoforms from four species of bivalves.

Heterogeneity and tissue specificity of tropomyosin isoforms obtained from four species of bivalves (Scapharca broughtonii (ark shell), Mytilus galloprovincialis (mussel), Atrina pectinata (surf clam) and Crassostrea gigas (Pacific oyster)), were examined. Tropomyosins were extracted from translucent and opaque portions of posterior adductor muscle, respectively, and cardiac muscle of each bivalve. There were two tropomyosin isoforms in the ark shell, the surf clam and the Pacific oyster. They were designated as TMa and TMb. In the ark shell, TMa was the common isoform and TMb was specific for the opaque portion of the adductor muscle. In the surf clam, TMb was the common isoform present in all tissues. TMa was found only in the translucent portion of muscle. In the Pacific oyster, TMb was the major component in both portions of adductor muscle and TMa was the major component in cardiac muscle, although both tropomyosins were included in all tissues. The mussel had only one tropomyosin.

Animals↗
PubMed2005

PKCalpha is involved in phorbol ester TPA-mediated stabilization of p14ARF.

We generated A21-13 cells expressing p14(ARF) in the presence of doxycycline in order to examine the stability of p14(ARF) protein. The effects of proteasome inhibitor MG132 on p14(ARF) protein stabilization were detectable using our experimental procedure. Introduction of mutant p53 did not affect MG132-mediated p14(ARF) protein stabilization. We found that phorbol ester TPA (12-o-tetradecanoyl-phorbol 13-acetate) stabilized p14(ARF) protein and that p53 status had no effect on TPA-mediated stabilization. TPA-mediated stabilization was abolished by staurosporine but not by lovastatin or U0126. We further investigated which isoforms of PKC were involved in TPA-mediated p14(ARF) stabilization using short-interference RNA. Knockdown of PKCalpha, but not PKCdelta, attenuated TPA-mediated p14(ARF) stabilization. These findings suggest that PKCalpha is involved in TPA-mediated stabilization of p14(ARF) protein, and this effect of TPA was not affected by the Ras/MAPK pathway or p53 status. Our results are indicative of a novel role of PKC in p14(ARF) protein stability.

Butadienes↗
PubMed2002

Nicorandil preserves mitochondrial function during ischemia in perfused rat heart.

A possible mechanism for the action of nicorandil on the improvement of energy metabolism of ischemic/reperfused hearts was examined. Perfused rat hearts were subjected to 35-min ischemia/60-min reperfusion. The heart was treated with nicorandil at concentrations of 10 to 100 microM for the last 30-min of pre-ischemia. Nicorandil preserved the mitochondrial oxygen consumption rate during ischemia and attenuated the decrease in mitochondrial function during reperfusion in association with the enhanced post-ischemic recovery of the left ventricular developed pressure. To assess the direct effect on mitochondria, myocardial saponin-skinned bundles were incubated under hypoxic conditions in vitro. Hypoxia-induced decrease in the mitochondrial oxygen consumption rate was attenuated by treatment of the bundles with 100 microM nicorandil. This attenuation was abolished by the combined treatment with the K(ATP) channel blocker, 5-hydroxydecanoate (5-HD). These results suggest that nicorandil is capable of attenuating ischemia/reperfusion injury of isolated perfused hearts through preservation of mitochondrial function during ischemia.

Animals↗
PubMed2002

Mitochondrial damage during ischemia determines post-ischemic contractile dysfunction in perfused rat heart.

Possible mechanisms underlying sodium overload-induced ischemia/reperfusion injury in perfused rat hearts were examined. Massive accumulation of myocardial Na(+) occurred during ischemia, suggesting cytosolic sodium overload in cardiac cells. Treatment of the pre-ischemic heart with 0.3 micromol/l tetrodotoxin or 3 micromol/l ethyl-isopropyl amiloride enhanced post-ischemic contractile recovery (72 or 82% of initial vs 24% for untreated group), which was associated with suppression of tissue Na(+) accumulation (138 or 141% of initial vs 270% for untreated group), restoration of tissue high-energy phosphates, and preservation of the ability of mitochondria to produce ATP in the ischemic/reperfused heart. The release of cytochrome c from the ischemic heart was observed, which was blocked by treatment of the pre-ischemic heart with these agents. The improvement of post-ischemic contractile recovery by these agents was closely correlated with the ability of mitochondria to produce ATP during ischemia. To examine the effects of sodium overload on mitochondrial function, isolated mitochondria were incubated in the presence of various concentrations of Na(+). Na(+) induced mitochondrial membrane perturbations such as depolarization of the membrane potential, mitochondrial swelling, cytochrome c release from isolated mitochondria, and a reduction in oxidative phosphorylation. These events in the isolated mitochondria were not blocked by the presence of the above agents. The results suggest that cytosolic sodium overload in cardiac cells may induce deterioration of the mitochondrial function during ischemia and that this mitochondrial damage may determine post-ischemic contractile dysfunction in perfused rat hearts.

Amiloride↗
PubMed2002

Sodium accumulation during ischemia induces mitochondrial damage in perfused rat hearts.

OBJECTIVE: The present study aimed to elucidate the involvement of sodium overload and following damage to mitochondria during ischemia in the genesis of ischemia/reperfusion injury of perfused rat hearts. METHODS: Isolated, perfused hearts were exposed to different durations (15-35 min) of ischemia followed by 60-min reperfusion. At the end of ischemia or reperfusion, myocardial sodium and calcium contents and myocardial high-energy phosphates were determined. The cardiac mitochondrial ability to produce ATP was measured using saponin-skinned bundles. The effects of sodium on the mitochondrial membrane potential and the oxidative phosphorylation rate were examined using isolated mitochondria from normal hearts. RESULTS: Post-ischemic recovery of left ventricular developed pressure decreased in an ischemic duration-dependent manner. Ischemia induced an increase in myocardial sodium, but not calcium. This increase was dependent on the duration of ischemia. The oxygen consumption rate of skinned bundles from the ischemic heart decreased at the end of ischemia. Incubation of mitochondria with various concentrations of sodium chloride or sodium lactate in vitro resulted in a depolarization of mitochondrial membrane potential and a decrease in ATP-generating activity. This decrease was not restored after elimination of sodium compounds. CONCLUSIONS: The present findings suggest that ischemia induces an increase in sodium influx from the extracellular space and that accumulated sodium may induce irreversible damage to mitochondria during ischemia. This mitochondrial dysfunction may be one of the most important determinants for the genesis of ischemia/reperfusion injury in perfused rat hearts.

Analysis of Variance↗
PubMed2002

Protective effect of propranolol on mitochondrial function in the ischaemic heart.

1. The present study was aimed to determine whether propranolol improves contractile function of the ischaemic/reperfused heart through protection of the mitochondrial function during ischaemia. 2. Isolated perfused rat hearts were subjected to 35-min ischaemia followed by 60-min reperfusion. Pre-treatment with propranolol at the concentrations of 10 to 100 microM for the final 3 min of pre-ischaemia resulted in the improvement of ischaemia/reperfusion-induced contractile dysfunction, release of creatine kinase (CK) into perfusate, and decrease in myocardial high-energy phosphates. Propranolol also attenuated ischaemia-induced accumulation in Na+, suggesting that cytosolic sodium overload during ischaemia was prevented by propranolol. 3. The mitochondrial oxygen consumption rate of skinned bundles from the perfused heart decreased at the end of ischaemia and it further decreased at the end of reperfusion. These decreases were cancelled by treatment with propranolol. A release of cytochrome c from the perfused heart was observed during ischaemia, and this release was suppressed by treatment with propranolol. 4. To elucidate the direct effect of propranolol on mitochondria, the mitochondria were isolated from normal hearts and their activities were determined in the presence of various concentrations of Na+ and propranolol. The addition of sodium lactate, which mimicked sodium overload in the ischaemic heart, reduced the state 3 respiration, whereas this reduction was not attenuated by the presence of propranolol. 5. These results suggest that cardioprotection of propranolol may be exerted via attenuating Na+ influx into cardiac cells followed by prevention of the mitochondrial dysfunction in the ischaemic heart, leading to improvement of energy production of the heart during reperfusion.

Adenosine Triphosphate↗
PubMed2002

Esophageal anthracosis: lesion mimicking malignant melanoma.

A case of anthracosis of the esophagus is reported. The patient was a previously healthy 69-year-old Japanese woman. A black and slightly elevated lesion was detected in her esophagus by upper gastroesophageal fiberoscopic examination. Endoscopically, the lesion looked like malignant melanoma. Thoracic esophagotomy was then performed. Histological examination revealed a pigmented lesion beneath the mucosal epithelial layer. The lesion consisted of an aggregation of histiocytes containing an abundance of tiny black pigments. A few mature lymphocytes and plasma cells were also evident in the periphery of the lesion. Histologically, these findings looked like lymph nodes in the pulmonary hilus; however, no lymph nodal structure was evident in the esophageal wall. Traction diverticula were also noted in the pigmented lesion. The patient has remained well without disease for 9 months since the surgery. Although anthracosis is a rare condition in the esophagus, the present case gave warning to pathologists and clinicians that it does indeed occur. Endoscopists and pathologists should differentiate anthracosis from malignant melanoma because the treatment and outcome are quite different for each.

Aged↗