Alterations in sarcoplasmic reticulum calcium-storing proteins in pressure-overload cardiac hypertrophy

Hiroyuki Tsutsui, Yuji Ishibashi, Kyoko Imanaka-Yoshida, Shimako Yamamoto, Toshimichi Yoshida, Masaru Sugimachi, Yoshitoshi Urabe, Akira Takeshita

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Abstract

The alterations of intracellular calcium (Ca2+) homeostasis may be responsible for the contractile defects in pressure-overload cardiac hypertrophy. The Ca2+-adenosinetriphosphatase (ATPase) protein level of the sarcoplasmic reticulum (SR) is reduced in the hypertrophied or failing heart. However, it is not known whether Ca2+ -storing proteins, including calsequestrin and calreticulin, are also altered during cardiac hypertrophy. We quantified SR Ca2+-regulatory proteins using Western blot analysis in left ventricular (LV) muscle isolated from sham-operated control rats (n = 6) and rats with pressure overload 4 wk after abdominal aortic constriction (n = 7). The contractile function of isolated LV myocytes, assessed by the sarcomere motion measured with laser diffraction, was depressed in aortic- constricted rats. The SR Ca2+-ATPase protein level was decreased to 56 ± 9% (SE) of the control value in hypertrophied myocardium (P < 0.01). The calsequestrin protein level was not altered, whereas calreticulin was increased by 120 ± 3% of the control value in aortic-constricted rats (P < 0.05). The alterations in SR Ca2+-regulatory proteins were equally observed in hypertrophied hearts even when the results were normalized using the amounts of myosin heavy chain proteins in each sample. Immunohistochemical staining of calsequestrin in the control heart showed cross striations at the Z lines, whereas calreticulin was hardly observed within myocytes but was intense within interstitial fibroblasts. In the hypertrophied heart, calreticulin was observed at the perinuclear region within the myocyte cytoplasm. These data indicate that pressure-overload cardiac hypertrophy causes the alterations in SR Ca2+-storing proteins as well as in Ca2+- ATPase, which may contribute to the contractile dysfunction of the hypertrophied myocytes.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume272
Issue number1 41-1
Publication statusPublished - Feb 20 1997

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Cardiomegaly
Sarcoplasmic Reticulum
Calreticulin
Calcium
Pressure
Calsequestrin
Muscle Cells
Proteins
Adenosine Triphosphatases
Sarcomeres
Myosin Heavy Chains
Left Ventricular Function
Constriction
Myocardium
Cytoplasm
Lasers
Homeostasis
Fibroblasts
Western Blotting
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Tsutsui, H., Ishibashi, Y., Imanaka-Yoshida, K., Yamamoto, S., Yoshida, T., Sugimachi, M., ... Takeshita, A. (1997). Alterations in sarcoplasmic reticulum calcium-storing proteins in pressure-overload cardiac hypertrophy. American Journal of Physiology - Heart and Circulatory Physiology, 272(1 41-1).

Alterations in sarcoplasmic reticulum calcium-storing proteins in pressure-overload cardiac hypertrophy. / Tsutsui, Hiroyuki; Ishibashi, Yuji; Imanaka-Yoshida, Kyoko; Yamamoto, Shimako; Yoshida, Toshimichi; Sugimachi, Masaru; Urabe, Yoshitoshi; Takeshita, Akira.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 272, No. 1 41-1, 20.02.1997.

Research output: Contribution to journalArticle

Tsutsui, H, Ishibashi, Y, Imanaka-Yoshida, K, Yamamoto, S, Yoshida, T, Sugimachi, M, Urabe, Y & Takeshita, A 1997, 'Alterations in sarcoplasmic reticulum calcium-storing proteins in pressure-overload cardiac hypertrophy', American Journal of Physiology - Heart and Circulatory Physiology, vol. 272, no. 1 41-1.
Tsutsui, Hiroyuki ; Ishibashi, Yuji ; Imanaka-Yoshida, Kyoko ; Yamamoto, Shimako ; Yoshida, Toshimichi ; Sugimachi, Masaru ; Urabe, Yoshitoshi ; Takeshita, Akira. / Alterations in sarcoplasmic reticulum calcium-storing proteins in pressure-overload cardiac hypertrophy. In: American Journal of Physiology - Heart and Circulatory Physiology. 1997 ; Vol. 272, No. 1 41-1.
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