Regulation of sarcoplasmic reticulum calcium pump gene expression by hindlimb unweighting

L. M. Schulte, Javier Navarro, S. C. Kandarian

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Hindlimb unweighting (HU) causes upregulation of several muscle-specific genes responsible for the slow-to-fast transition in soleus skeletal muscle properties despite the profound muscle atrophy. The purpose of this study was to examine the expression of the fast and slow isoforms of the sarcoplasmic reticulum Ca2+-ATPase at the mRNA and protein level in the soleus muscle over a time course of HU and relate them to Ca2+-dependent ATPase activity and selected contractile properties. mRNA levels of the acetylcholine receptor (AChR) were measured to compare the signal of unweighting with denervation. Atrophy of the soleus muscles from tail-suspended rats was observed at all time points with muscle mass decreased by 52% at 28 days of HU (P < 0.05). Northern blot analysis showed the relative expression of the fast Ca2+ pump mRNA increased by 0, 250, 910, 1,340, and 4,050% over control levels at 1, 4, 7, 14, and 28 days of HU, respectively, whereas changes in slow mRNA were variable and modest in comparison. For the same time points, Western blot analysis showed relative expression of the fast Ca2+ pump protein increased by 30, 110, 320, 280, and 300% over control levels, whereas the slow-pump protein expression was unchanged except for a 75% decrease at 28 days of HU. Specific Ca2+-dependent ATPase activity was increased (P < 0.05) by 170% at 28 days of HU. Contractile properties measured in vitro at 14 and 28 days revealed time to peak tension and one- half relaxation time were shortened (P < 0.05) and a rightward shift in the tension-frequency curves in unloaded soleus muscles. In contrast to denervation, no increase in AChR mRNA was detected in the HU time course. These results indicate HU can dramatically upregulate the expression of the fast isoform of the Ca2+ pump and its related functional properties. Additionally, the triggering signal of unloading is distinct from the loss of innervation.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Cell Physiology
Volume264
Issue number5 33-5
StatePublished - 1993
Externally publishedYes

Fingerprint

Sarcoplasmic Reticulum
Hindlimb
Gene expression
Muscle
Pumps
Calcium
Gene Expression
Skeletal Muscle
Messenger RNA
Calcium-Transporting ATPases
Level control
Cholinergic Receptors
Denervation
Adenosine Triphosphatases
Protein Isoforms
Up-Regulation
Proteins
Muscles
Muscular Atrophy
Unloading

Keywords

  • calcium adenosine- triphosphatase
  • isometric twitch
  • non-weight bearing
  • skeletal muscle
  • soleus

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

Regulation of sarcoplasmic reticulum calcium pump gene expression by hindlimb unweighting. / Schulte, L. M.; Navarro, Javier; Kandarian, S. C.

In: American Journal of Physiology - Cell Physiology, Vol. 264, No. 5 33-5, 1993.

Research output: Contribution to journalArticle

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abstract = "Hindlimb unweighting (HU) causes upregulation of several muscle-specific genes responsible for the slow-to-fast transition in soleus skeletal muscle properties despite the profound muscle atrophy. The purpose of this study was to examine the expression of the fast and slow isoforms of the sarcoplasmic reticulum Ca2+-ATPase at the mRNA and protein level in the soleus muscle over a time course of HU and relate them to Ca2+-dependent ATPase activity and selected contractile properties. mRNA levels of the acetylcholine receptor (AChR) were measured to compare the signal of unweighting with denervation. Atrophy of the soleus muscles from tail-suspended rats was observed at all time points with muscle mass decreased by 52{\%} at 28 days of HU (P < 0.05). Northern blot analysis showed the relative expression of the fast Ca2+ pump mRNA increased by 0, 250, 910, 1,340, and 4,050{\%} over control levels at 1, 4, 7, 14, and 28 days of HU, respectively, whereas changes in slow mRNA were variable and modest in comparison. For the same time points, Western blot analysis showed relative expression of the fast Ca2+ pump protein increased by 30, 110, 320, 280, and 300{\%} over control levels, whereas the slow-pump protein expression was unchanged except for a 75{\%} decrease at 28 days of HU. Specific Ca2+-dependent ATPase activity was increased (P < 0.05) by 170{\%} at 28 days of HU. Contractile properties measured in vitro at 14 and 28 days revealed time to peak tension and one- half relaxation time were shortened (P < 0.05) and a rightward shift in the tension-frequency curves in unloaded soleus muscles. In contrast to denervation, no increase in AChR mRNA was detected in the HU time course. These results indicate HU can dramatically upregulate the expression of the fast isoform of the Ca2+ pump and its related functional properties. Additionally, the triggering signal of unloading is distinct from the loss of innervation.",
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N2 - Hindlimb unweighting (HU) causes upregulation of several muscle-specific genes responsible for the slow-to-fast transition in soleus skeletal muscle properties despite the profound muscle atrophy. The purpose of this study was to examine the expression of the fast and slow isoforms of the sarcoplasmic reticulum Ca2+-ATPase at the mRNA and protein level in the soleus muscle over a time course of HU and relate them to Ca2+-dependent ATPase activity and selected contractile properties. mRNA levels of the acetylcholine receptor (AChR) were measured to compare the signal of unweighting with denervation. Atrophy of the soleus muscles from tail-suspended rats was observed at all time points with muscle mass decreased by 52% at 28 days of HU (P < 0.05). Northern blot analysis showed the relative expression of the fast Ca2+ pump mRNA increased by 0, 250, 910, 1,340, and 4,050% over control levels at 1, 4, 7, 14, and 28 days of HU, respectively, whereas changes in slow mRNA were variable and modest in comparison. For the same time points, Western blot analysis showed relative expression of the fast Ca2+ pump protein increased by 30, 110, 320, 280, and 300% over control levels, whereas the slow-pump protein expression was unchanged except for a 75% decrease at 28 days of HU. Specific Ca2+-dependent ATPase activity was increased (P < 0.05) by 170% at 28 days of HU. Contractile properties measured in vitro at 14 and 28 days revealed time to peak tension and one- half relaxation time were shortened (P < 0.05) and a rightward shift in the tension-frequency curves in unloaded soleus muscles. In contrast to denervation, no increase in AChR mRNA was detected in the HU time course. These results indicate HU can dramatically upregulate the expression of the fast isoform of the Ca2+ pump and its related functional properties. Additionally, the triggering signal of unloading is distinct from the loss of innervation.

AB - Hindlimb unweighting (HU) causes upregulation of several muscle-specific genes responsible for the slow-to-fast transition in soleus skeletal muscle properties despite the profound muscle atrophy. The purpose of this study was to examine the expression of the fast and slow isoforms of the sarcoplasmic reticulum Ca2+-ATPase at the mRNA and protein level in the soleus muscle over a time course of HU and relate them to Ca2+-dependent ATPase activity and selected contractile properties. mRNA levels of the acetylcholine receptor (AChR) were measured to compare the signal of unweighting with denervation. Atrophy of the soleus muscles from tail-suspended rats was observed at all time points with muscle mass decreased by 52% at 28 days of HU (P < 0.05). Northern blot analysis showed the relative expression of the fast Ca2+ pump mRNA increased by 0, 250, 910, 1,340, and 4,050% over control levels at 1, 4, 7, 14, and 28 days of HU, respectively, whereas changes in slow mRNA were variable and modest in comparison. For the same time points, Western blot analysis showed relative expression of the fast Ca2+ pump protein increased by 30, 110, 320, 280, and 300% over control levels, whereas the slow-pump protein expression was unchanged except for a 75% decrease at 28 days of HU. Specific Ca2+-dependent ATPase activity was increased (P < 0.05) by 170% at 28 days of HU. Contractile properties measured in vitro at 14 and 28 days revealed time to peak tension and one- half relaxation time were shortened (P < 0.05) and a rightward shift in the tension-frequency curves in unloaded soleus muscles. In contrast to denervation, no increase in AChR mRNA was detected in the HU time course. These results indicate HU can dramatically upregulate the expression of the fast isoform of the Ca2+ pump and its related functional properties. Additionally, the triggering signal of unloading is distinct from the loss of innervation.

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