Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure

Keiko Igarashi-Saito, Hiroyuki Tsutsui, Shimako Yamamoto, Masaru Takahashi, Shintaro Kinugawa, Hirofumit Agawa, Makotq Usui, Mitsutaka Yamamoto, Kensuke Egashira, Akira Takeshita

研究成果: ジャーナルへの寄稿記事

18 引用 (Scopus)

抄録

Sarcoülasmic reticulurn (SR) Ca 2+ -ATPase gene expression is reduced in the failing myocardium. However, the functional relevance of these changes to myocardial contractility is not yet established. We assessed myocardial contractile function by analyzing sarcomere motion of isolated myocytes and also quantified SR Ca 2+ regulatory protein gene expression by Northern blot analysis in the same hearts obtained from 10 dogs with pacing-induced heart failure (HF; 240 beats/min, 4 wk) and 7 control dogs. Sarcomere-shortening velocity was depressed in HF myocytes, accompanied by the prolongation of intracellular Ca 2+ concentration ([Ca 2+ ]j) transient measured by indo 1 fluorescence ratio. SR Ca 2+ -ATPase mRNA levels (normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA) were significantly depressed in HF, and calsequestrin mRNA was increased. For control and HF dogs, sarcomere-shortening velocity correlated positively with Ca 2+ -ATPase mRNA levels (r = 0.73, n = 17, P < 0.01) but not with calsequestrin mRNA. Ca2"l"-ATPase mRNA levels were correlated with 45Ca 2+ uptake rate by SR, which was also reduced in HF. Moreover, the inhibition of SR Ca 2+ -ATPase with thapsigargin or cyclopiazonic acid reproduced in normal myocytes the abnormalities observed in HF myocytes, such as depressed contractility and the prolonged [Ca2t]j transient duration. A downregulation of Ca 2+ -ATPase gene expression and a resultant decrease in Ca2t uptake by SR may be responsible for the contractile dysfunction and the alterations of [Ca 2+ ]j transient in HF.

元の言語英語
ジャーナルAmerican Journal of Physiology
275
発行部数1 PART 2
出版物ステータス出版済み - 12 1 1998

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Tachycardia
Muscle Cells
Adenosine Triphosphatases
Heart Failure
Messenger RNA
Sarcomeres
Calsequestrin
Dogs
Gene Expression
Glyceraldehyde-3-Phosphate Dehydrogenases
Thapsigargin
Calcium-Transporting ATPases
Regulator Genes
Northern Blotting
Myocardium
Down-Regulation
Fluorescence
Proteins

All Science Journal Classification (ASJC) codes

  • Physiology (medical)

これを引用

Igarashi-Saito, K., Tsutsui, H., Yamamoto, S., Takahashi, M., Kinugawa, S., Agawa, H., ... Takeshita, A. (1998). Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure American Journal of Physiology, 275(1 PART 2).

Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure . / Igarashi-Saito, Keiko; Tsutsui, Hiroyuki; Yamamoto, Shimako; Takahashi, Masaru; Kinugawa, Shintaro; Agawa, Hirofumit; Usui, Makotq; Yamamoto, Mitsutaka; Egashira, Kensuke; Takeshita, Akira.

:: American Journal of Physiology, 巻 275, 番号 1 PART 2, 01.12.1998.

研究成果: ジャーナルへの寄稿記事

Igarashi-Saito, K, Tsutsui, H, Yamamoto, S, Takahashi, M, Kinugawa, S, Agawa, H, Usui, M, Yamamoto, M, Egashira, K & Takeshita, A 1998, ' Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure ', American Journal of Physiology, 巻. 275, 番号 1 PART 2.
Igarashi-Saito K, Tsutsui H, Yamamoto S, Takahashi M, Kinugawa S, Agawa H その他. Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure American Journal of Physiology. 1998 12 1;275(1 PART 2).
Igarashi-Saito, Keiko ; Tsutsui, Hiroyuki ; Yamamoto, Shimako ; Takahashi, Masaru ; Kinugawa, Shintaro ; Agawa, Hirofumit ; Usui, Makotq ; Yamamoto, Mitsutaka ; Egashira, Kensuke ; Takeshita, Akira. / Role of SR Ca 2+ -ATPase in contractile dysfunction of myocytes in tachycardia-induced heart failure :: American Journal of Physiology. 1998 ; 巻 275, 番号 1 PART 2.
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abstract = "Sarco{\"u}lasmic reticulurn (SR) Ca 2+ -ATPase gene expression is reduced in the failing myocardium. However, the functional relevance of these changes to myocardial contractility is not yet established. We assessed myocardial contractile function by analyzing sarcomere motion of isolated myocytes and also quantified SR Ca 2+ regulatory protein gene expression by Northern blot analysis in the same hearts obtained from 10 dogs with pacing-induced heart failure (HF; 240 beats/min, 4 wk) and 7 control dogs. Sarcomere-shortening velocity was depressed in HF myocytes, accompanied by the prolongation of intracellular Ca 2+ concentration ([Ca 2+ ]j) transient measured by indo 1 fluorescence ratio. SR Ca 2+ -ATPase mRNA levels (normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA) were significantly depressed in HF, and calsequestrin mRNA was increased. For control and HF dogs, sarcomere-shortening velocity correlated positively with Ca 2+ -ATPase mRNA levels (r = 0.73, n = 17, P < 0.01) but not with calsequestrin mRNA. Ca2{"}l{"}-ATPase mRNA levels were correlated with 45Ca 2+ uptake rate by SR, which was also reduced in HF. Moreover, the inhibition of SR Ca 2+ -ATPase with thapsigargin or cyclopiazonic acid reproduced in normal myocytes the abnormalities observed in HF myocytes, such as depressed contractility and the prolonged [Ca2t]j transient duration. A downregulation of Ca 2+ -ATPase gene expression and a resultant decrease in Ca2t uptake by SR may be responsible for the contractile dysfunction and the alterations of [Ca 2+ ]j transient in HF.",
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AU - Igarashi-Saito, Keiko

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AU - Yamamoto, Shimako

AU - Takahashi, Masaru

AU - Kinugawa, Shintaro

AU - Agawa, Hirofumit

AU - Usui, Makotq

AU - Yamamoto, Mitsutaka

AU - Egashira, Kensuke

AU - Takeshita, Akira

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N2 - Sarcoülasmic reticulurn (SR) Ca 2+ -ATPase gene expression is reduced in the failing myocardium. However, the functional relevance of these changes to myocardial contractility is not yet established. We assessed myocardial contractile function by analyzing sarcomere motion of isolated myocytes and also quantified SR Ca 2+ regulatory protein gene expression by Northern blot analysis in the same hearts obtained from 10 dogs with pacing-induced heart failure (HF; 240 beats/min, 4 wk) and 7 control dogs. Sarcomere-shortening velocity was depressed in HF myocytes, accompanied by the prolongation of intracellular Ca 2+ concentration ([Ca 2+ ]j) transient measured by indo 1 fluorescence ratio. SR Ca 2+ -ATPase mRNA levels (normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA) were significantly depressed in HF, and calsequestrin mRNA was increased. For control and HF dogs, sarcomere-shortening velocity correlated positively with Ca 2+ -ATPase mRNA levels (r = 0.73, n = 17, P < 0.01) but not with calsequestrin mRNA. Ca2"l"-ATPase mRNA levels were correlated with 45Ca 2+ uptake rate by SR, which was also reduced in HF. Moreover, the inhibition of SR Ca 2+ -ATPase with thapsigargin or cyclopiazonic acid reproduced in normal myocytes the abnormalities observed in HF myocytes, such as depressed contractility and the prolonged [Ca2t]j transient duration. A downregulation of Ca 2+ -ATPase gene expression and a resultant decrease in Ca2t uptake by SR may be responsible for the contractile dysfunction and the alterations of [Ca 2+ ]j transient in HF.

AB - Sarcoülasmic reticulurn (SR) Ca 2+ -ATPase gene expression is reduced in the failing myocardium. However, the functional relevance of these changes to myocardial contractility is not yet established. We assessed myocardial contractile function by analyzing sarcomere motion of isolated myocytes and also quantified SR Ca 2+ regulatory protein gene expression by Northern blot analysis in the same hearts obtained from 10 dogs with pacing-induced heart failure (HF; 240 beats/min, 4 wk) and 7 control dogs. Sarcomere-shortening velocity was depressed in HF myocytes, accompanied by the prolongation of intracellular Ca 2+ concentration ([Ca 2+ ]j) transient measured by indo 1 fluorescence ratio. SR Ca 2+ -ATPase mRNA levels (normalized to glyceraldehyde-3-phosphate dehydrogenase mRNA) were significantly depressed in HF, and calsequestrin mRNA was increased. For control and HF dogs, sarcomere-shortening velocity correlated positively with Ca 2+ -ATPase mRNA levels (r = 0.73, n = 17, P < 0.01) but not with calsequestrin mRNA. Ca2"l"-ATPase mRNA levels were correlated with 45Ca 2+ uptake rate by SR, which was also reduced in HF. Moreover, the inhibition of SR Ca 2+ -ATPase with thapsigargin or cyclopiazonic acid reproduced in normal myocytes the abnormalities observed in HF myocytes, such as depressed contractility and the prolonged [Ca2t]j transient duration. A downregulation of Ca 2+ -ATPase gene expression and a resultant decrease in Ca2t uptake by SR may be responsible for the contractile dysfunction and the alterations of [Ca 2+ ]j transient in HF.

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