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113 results on '"Iwasawa, Kuniaki"'

1. Interpretations of SARS-CoV-2 IgM and IgG antibody titers in the seroepidemiological study of asymptomatic healthy volunteers

Author

Mitani, Akihisa, Horie, Takeshi, Yokoyama, Rin, Nakano, Yuki, Hamada, Kensuke, Inoue, Yukiko, Saito, Minako, Ishii, Takashi, Sunohara, Mitsuhiro, Takahashi, Ryota, Usui, Tomoko, Emoto, Noriko, Nishimoto, Nahoko, Murano, Yoko, Okazaki, Sachiko, Tateishi, Shoko, Iwasawa, Kuniaki, Yao, Atsushi, Kurano, Makoto, Yatomi, Yutaka, and Yanagimoto, Shintaro

Published
2022
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11. Sarcolemmal fragility secondary to the degradation of dystrophin in dilated cardiomyopathy, as estimated by electron microscopy

Author

Kawada, Tomie, Hemmi, Chieko, Fukuda, Satoru, Tezuka, Asaki, Iwasawa, Kuniaki, Nakazawa, Mikio, Sato, Hiroshi, and Toyo-oka, Teruhiko

Subjects
Experimental Cardiology
Abstract

A common gene deletion or mutation of delta-sarcoglycan (delta-SG) in dystrophin-related proteins (DRPs) is identified in both TO-2 strain hamsters and human families with dilated cardiomyopathy. We have succeeded in the long-lasting in vivo supplementation of a normal delta-SG gene by recombinant adeno-associated virus vector, restoration of the morphological and functional degeneration, and improvement in the prognosis of the TO-2 hamster. To evaluate the integrity of the sarcolemma (SL) and the subsequent change of organelles in cardiomyocytes of the TO-2 strain hamster, we examined electron microscopy (EM) images focusing on the sarcolemmal stability at the end stage of heart failure. Two types of sarcolemmal degradation were detected: the widened and locally thickened SL, and blurred and discontinuous SL. Bizarrely formed mitochondria of varying sizes were also observed. Immuno-EM revealed clear expression of dystrophin in the SL and intense expression at the costamere as well as at the T-tubules in the control F1B strain hearts, but a patchy deposition of dystrophin was observed along the SL without the transgene of delta-SG. In contrast to the previous reports that dystrophin's integrity was intact, the present results suggest that the gene deletion of delta-SG and the loss of delta-SG protein in the SL cardioselectively cause the morphological and functional deterioration of dystrophin and the resultant instability of the SL. The sarcolemmal fragility may be similar to Duchenne-type progressive muscular dystrophy in skeletal muscle. In addition to the mechanical role, another aspect of DRPs for the intracellular signal transmission is also discussed.

Published
2003

12. Antiarrhythmic effect and its underlying ionic mechanism of 17β-estradiol in cardiac myocytes

Author

Nakajima, Toshiaki, Iwasawa, Kuniaki, Oonuma, Hitoshi, Morita, Toshihiro, Goto, Atsuro, Wang, Yuepeng, and Hazama, Hisanori

Subjects
Cardiotonic Agents, Patch-Clamp Techniques, Calcium Channels, L-Type, Estradiol, Pyridines, Myocardium, Guinea Pigs, Estrogen Antagonists, Isoproterenol, Action Potentials, Heart, In Vitro Techniques, Membrane Potentials, Piperidines, Papers, Androgens, Potassium Channel Blockers, Animals, Female, Calcium Channels, Estrogens, Non-Steroidal, Anti-Arrhythmia Agents
Abstract

1. The effects of oestrogens on action potential and membrane currents were examined in single guinea-pig atrial myocytes. 2. 17Beta-estradiol (3-10 microM) shortened the action potential duration without significant changes in the resting membrane potential. E-4031 (1 microM) markedly prolonged the action potential duration and induced early afterdepolarization, and 17beta-estradiol (10 microM) abolished it. 3. When cells were perfused in isoproterenol-containing solution, action potentials due to abnormal automaticity caused by membrane depolarization developed, and were also inhibited by 17beta-estradiol. 4. Under voltage clamp conditions, the voltage-dependent Ca2+ currents consisted of both T-(I(Ca,T)) and L-type (I(Ca,L)). 17Beta-estradiol reduced I(Ca,L) concentration-dependently, while it (10 microM) suppressed I(Ca,T) only by approximately 10%. 17Beta-estradiol did not affect time courses of I(Ca,L) inactivation, but it shifted the steady-state inactivation curve to more negative potentials. 5. 17Beta-estradiol (10 microM) did not affect the time-dependent K+ current (I(K)), referred to as I(Kr) and I(Ks) and inwardly rectifying K+ current. However, 17beta-estradiol (30 microM) or diethylstilbestrol (10 microM) inhibited K+ currents. 6. DES and ethinylestradiol (EES) also suppressed I(Ca,L), but testosterone and progesterone failed to inhibit I(Ca,L) The potency of the inhibitory effect on I(Ca,L) was DESEES17beta-estradiol. 7. 17Beta-estradiol and DES also inhibited the cyclic AMP-enhanced I(Ca,L), but cyclic GMP in the pipette or pretreatment of L-NAME could not block the effects of oestrogen on I(Ca,L). 8 These results suggest that oestrogen specifically has antiarrhythmic effects, possibly by acting the L-type Ca2+ channels. The antiarrhythmic effects of oestrogens may contribute to the cardioprotective actions of oestrogens.

Published
1999

13. Inhibitory effects of ω-3 polyunsaturated fatty acids on receptor-mediated non-selective cation currents in rat A7r5 vascular smooth muscle cells

Author

Asano, Michiko, Nakajima, Toshiaki, Iwasawa, Kuniaki, Hazama, Hisanori, Omata, Masao, Soma, Masaaki, Yamashita, Kamejiro, and Okuda, Yukichi

Subjects
Guanosine 5'-O-(3-Thiotriphosphate), Papers, Fatty Acids, Omega-3, Animals, Receptors, Cell Surface, Ion Channels, Muscle, Smooth, Vascular, Cell Line, Rats
Abstract

1. The effects of omega-3 polyunsaturated fatty acids on receptor-mediated non-selective cation current (Icat) and K+ current were investigated in aortic smooth muscle cells from foetal rat aorta (A7r5 cells). The whole-cell voltage clamp technique was employed. 2. With a K(+)-containing solution, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA, 30 microM) produced an outward current at a holding potential of -40 mV. This response was inhibited by tetraethylammonium (20 mM) or Cs+ in the patch pipette solution, and the reversal potential of the EPA-induced current followed the K+ equilibrium potential in a near Nernstian manner. 3. Under conditions with a Cs(+)-containing pipette solution, both vasopressin and endothelin-1 (100 nM) induced a long-lasting inward current at a holding potential of -60 mV. The reversal potential of these agonist-induced currents was about +0 mV, and was not significantly altered by the replacement of the extracellular or intracellular Cl+ concentration, suggesting that the induced current was a cation-selective current (Icat). 4. La3+ and Cd2+ (1 mM) completely abolished these agonist-induced Icat, but nifedipine (10 microM) failed to inhibit it significantly. 5. omega-3 polyunsaturated fatty acids (3-100 microM), EPA, DHA and docosapentaenoic acids (DPA), inhibited the agonist-induced Icat in a concentration-dependent manner. The potency of the inhibitory effect was EPADHADPA, and the half maximal inhibitory concentration (IC50) of EPA was about 7 microM. 6. Arachidonic and linoleic acids (10, 30 microM) showed a smaller inhibitory effect compared to omega-3 fatty acids. Also, oleic and stearic acids (30 microM) did not show a significant inhibitory effect on Icat. 7. A similar inhibitory action of EPA was observed when Icat was activated by intracellularly applied GTP gamma S in the absence of agonists, suggesting that the site of action of omega-3 fatty acids is not located on the receptor. 8. These results demonstrate that omega-3 polyunsaturated fatty acids can activate a K+ current and also effectively inhibit receptor-mediated non-selective cation currents in rat A7r5 vascular smooth muscle cells. Thus, the data suggest that omega-3 fatty acids may play an important role in the regulation of vascular tone.

Published
1997

18. Acute and chronic effects of eicosapentaenoic acid on voltage-gated sodium channel expressed in cultured human bronchial smooth muscle cells

Author

Jo, Taisuke, primary, Iida, Haruko, additional, Kishida, Shinya, additional, Imuta, Hiroyuki, additional, Oonuma, Hitoshi, additional, Nagata, Taiji, additional, Hara, Hajime, additional, Iwasawa, Kuniaki, additional, Soma, Masaaki, additional, Sato, Yoshiaki, additional, Nagase, Takahide, additional, Nagai, Ryozo, additional, and Nakajima, Toshiaki, additional

Published
2005
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20. Effects of Colforsin Daropate Hydrochloride (Adehl Inj.), Anti-Acute Heart Failure Agent, on Adenylate Cyclase-Related Hormone Actions

Author

TAMAKI, Satoru, primary, HOSODA, Saichi, additional, ISHIKAWA, Yoshihiro, additional, FUJIHARA, Ryo, additional, HASUNUMA, Tomoko, additional, NAKAMURA, Masahiko, additional, IWASAWA, Kuniaki, additional, YAMASHITA, Hiroshi, additional, MATSUDA, Hiroyuki, additional, KUROSU, Tetsuya, additional, UEBABA, Kazuo, additional, and KOMIYAMA, Kanki, additional

Published
2004
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21. Cell Density and Growth-dependent Down-regulation of Both Intracellular Calcium Responses to Agonist Stimuli and Expression of Smooth-surfaced Endoplasmic Reticulum in MC3T3-E1 Osteoblast-like Cells

Author

Koizumi, Toshiyuki, primary, Hikiji, Hisako, additional, Shin, Wee Soo, additional, Takato, Tsuyoshi, additional, Fukuda, Satoru, additional, Abe, Takahiro, additional, Koshikiya, Noboru, additional, Iwasawa, Kuniaki, additional, and Toyo-oka, Teruhiko, additional

Published
2003
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28. Enhancement of Endothelial Nitric Oxide Production by Chenodeoxycholic Acids in Patients with Hepatobiliary Diseases.

Author

Chisaki, Keigo, primary, Nakajima, Toshiaki, additional, Iwasawa, Kuniaki, additional, Iida, Haruko, additional, Matsumoto, Akihiro, additional, Tada, Minoru, additional, Komatsu, Yutaka, additional, Hirose, Ken, additional, Miyamoto, Kenichi, additional, Okuda, Yukichi, additional, Shiratori, Yasushi, additional, Goto, Atsuo, additional, Hirata, Yasunobu, additional, Nagai, Ryozo, additional, and Omata, Masao, additional

Published
2001
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30. Bile acids increase intracellular Ca2+concentration and nitric oxide production in vascular endothelial cells

Author

Nakajima, Toshiaki, primary, Okuda, Yukichi, additional, Chisaki, Keigo, additional, Shin, Wee-Soo, additional, Iwasawa, Kuniaki, additional, Morita, Toshihiro, additional, Matsumoto, Akihiro, additional, Suzuki, Jun-ichi, additional, Suzuki, Seizi, additional, Yamada, Nobuhiro, additional, Toyo-oka, Teruhiko, additional, Nagai, Ryozo, additional, and Omata, Masao, additional

Published
2000
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32. Eicosapentaenoic acid inhibits vasopressin-activated Ca2+ influx and cell proliferation in rat aortic smooth muscle cell lines

Author

Asano, Michiko, primary, Nakajima, Toshiaki, additional, Iwasawa, Kuniaki, additional, Asakura, Yukari, additional, Morita, Toshihiro, additional, Nakamura, Fumitaka, additional, Tomaru, Takanobu, additional, Wang, Yuepeng, additional, Goto, Atsuro, additional, Toyo-oka, Teruhiko, additional, Soma, Masaaki, additional, Suzuki, Seiji, additional, and Okuda, Yukichi, additional

Published
1999
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33. Troglitazone Inhibits Voltage-Dependent Calcium Currents in Guinea Pig Cardiac Myocytes

Author

Nakajima, Toshiaki, primary, Iwasawa, Kuniaki, additional, Oonuma, Hitoshi, additional, Imuta, Hiroyuki, additional, Hazama, Hisanori, additional, Asano, Michiko, additional, Morita, Toshihiro, additional, Nakamura, Fumitaka, additional, Suzuki, Jun-ichi, additional, Suzuki, Seiji, additional, Kawakami, Yasushi, additional, Omata, Masao, additional, and Okuda, Yukichi, additional

Published
1999
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36. ω-3 Polyunsaturated fatty acids—modulation of voltage-dependent L-type Ca2+ current in guinea-pig tracheal smooth muscle cells

Author

Hazama, Hisanori, primary, Nakajima, Toshiaki, additional, Asano, Michiko, additional, Iwasawa, Kuniaki, additional, Morita, Toshihiro, additional, Igarashi, Kouichi, additional, Nagata, Taiji, additional, Horiuchi, Tadashi, additional, Suzuki, Junichi, additional, Soma, Masaaki, additional, and Okuda, Yukichi, additional

Published
1998
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37. Influence of cellular incorporation of n-3 eicosapentaenoic acid on intracellular Ca2+ concentration and membrane potential in vascular smooth muscle cells

Author

Asano, Michiko, primary, Nakajima, Toshiaki, additional, Hazama, Hisanori, additional, Iwasawa, Kuniaki, additional, Tomaru, Takanobu, additional, Omata, Masao, additional, Soma, Masaaki, additional, Asakura, Yukari, additional, Mizutani, Masakazu, additional, Suzuki, Seiji, additional, Yamashita, Kamejiro, additional, and Okuda, Yukichi, additional

Published
1998
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50. Molecular and pharmacological characteristics of transient voltage-dependent K+ currents in cultured human pulmonary arterial smooth muscle cells.

Author

Iida, Haruko, Jo, Taisuke, Iwasawa, Kuniaki, Morita, Toshihiro, Hikiji, Hisako, Takato, Tsuyoshi, Toyo-oka, Teruhiko, Nagai, Ryozo, and Nakajima, Toshiaki

Subjects
SMOOTH muscle, PULMONARY artery, ARTERIES, PULMONARY blood vessels, MUSCLES
Abstract

The A-type voltage-dependent K+ current (IA) has been identified in several types of smooth muscle cells including the pulmonary artery (PA), but little is known about the pharmacological and molecular characteristics of IA in human pulmonary arterial smooth muscle cells (hPASMCs). We investigated IA expressed in cultured PASMCs isolated from the human main pulmonary artery, using patch-clamp techniques, reverse transcriptase–polymerase chain reaction (RT–PCR), quantitative real-time RT–PCR and immunocytochemical studies.With high EGTA and ATP in the pipette, the outward currents were dominated by a transient K+ current (IA), followed by a relatively small sustained outward current (IK).IA was inhibited by 4-aminopyridine (4-AP) concentration-dependently, and could be separated pharmacologically into two components by tetraethylammonium (TEA) sensitivity. A component was sensitive to TEA, and the second component was insensitive to TEA.IA was inhibited by blood depressing substrate (BDS)-II, a specific blocker of KV3.4 subunit, and phrixotoxin-II, a specific blocker of KV4.2 and 4.3.Flecainide inhibited IA concentration-dependently, but it inhibited it preferentially in the presence of TEA (TEA-insensitive IA).Systematic screening of expression of KV genes using RT–PCR showed the definite presence of transcripts of the IA-encoding genes for KV3.4, KV4.1, KV4.2 and KV4.3 as well as the IK-encoding genes for KV1.1, KV1.5 and KV2.1. The real-time RT–PCR analysis showed that the relative abundance of the encoding genes of IA α-subunit and KV channel-interacting proteins (KChIPs) was KV4.2>KV3.4>KV4.3 (long)>KV4.1, and KChIP3≫KChIP2, respectively.The presence of KV3.4, KV4.2 and KV4.3 proteins was also demonstrated by immunocytochemical studies, and confirmed by immunohistochemical staining using intact human PA sections.These results suggest that IA in cultured hPASMCs consists of two kinetically and pharmacologically distinct components, probably KV3.4 and KV4 channels.British Journal of Pharmacology (2005) 146, 49–59. doi:10.1038/sj.bjp.0706285; published online 6 June 2005 [ABSTRACT FROM AUTHOR]

Published
2005
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