scholarly journals Electrical stimulation of C2C12 myotubes induces contractions and represses thyroid-hormone-dependent transcription of the fast-type sarcoplasmic-reticulum Ca2+-ATPase gene

1997 ◽  
Vol 321 (3) ◽  
pp. 845-848 ◽  
Author(s):  
Marc H. M. THELEN ◽  
Warner S. SIMONIDES ◽  
Cornelis van HARDEVELD
Keyword(s):  
Electrical Stimulation ◽  
Thyroid Hormone ◽  
Sarcoplasmic Reticulum ◽  
Contractile Activity ◽  
Motor Nerve ◽  
C2c12 Myotubes ◽  
Transcriptional Level ◽  
Regulation Of Expression ◽  
Atpase Gene ◽  
Stimulation Of

Chronic low-frequency contraction of skeletal muscle, either induced by a slow motor nerve or through direct electrical stimulation, generally induces expression of proteins associated with the slow phenotype, while repressing the corresponding fast isoforms. Contractions thereby counteract the primarily transcriptional effect of thyroid hormone (T3), which results in the selective induction and stimulation of expression of fast isoforms. We studied the regulation of expression of the fast-type sarcoplasmic-reticulum Ca2+-ATPase (SERCA1), a characteristic component of the fast phenotype. Previous work suggested that reduction of SERCA1 expression by contractile activity might result from interference with the T3-dependent transcriptional stimulation of the SERCA1 gene. The present study was set up to test this unexpected mode of action of contractile activity. We show that electrical stimulation of C2C12 mouse myotubes, which results in synchronous contractions at the imposed frequency, reduces basal but virtually abolishes T3-dependent SERCA1 expression. T3-dependent expression of a reporter gene driven by the SERCA1 promoter was similarly affected by electrical stimulation. This is the first demonstration that the counteracting effects on muscle gene expression of electrically induced contractions and T3 may interact at the transcriptional level.

ATP concentrations and muscle tension increase linearly with muscle contraction

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Muscle Contraction ◽  
Motor Nerve ◽  
Muscle Tension ◽  
Nerve Fibers ◽  
Ventral Root ◽  
Ventral Roots ◽  
Root Stimulation ◽  
Stimulation Of

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

Simple micropatterning method for enhancing fusion efficiency and responsiveness to electrical stimulation of C2C12 myotubes

2014 ◽  
Vol 31 (1) ◽  
pp. 220-225 ◽  
Author(s):  
Yuzo Takayama ◽  
Akira Wagatsuma ◽  
Takayuki Hoshino ◽  
Kunihiko Mabuchi
Keyword(s):  
Electrical Stimulation ◽  
C2c12 Myotubes ◽  
Fusion Efficiency ◽  
Stimulation Of

Na(+)-K(+)-ATPase gene expression in rat intestine and Caco-2 cells: response to thyroid hormone

1993 ◽  
Vol 265 (4) ◽  
pp. G775-G782 ◽  
Author(s):  
R. A. Giannella ◽  
J. Orlowski ◽  
M. L. Jump ◽  
J. B. Lingrel
Keyword(s):  
Thyroid Hormone ◽  
Epithelial Cells ◽  
Enzymatic Activity ◽  
Intestinal Epithelial Cells ◽  
Blot Hybridization ◽  
Intestinal Cell ◽  
Transcriptional Level ◽  
Intestinal Epithelial ◽  
Subunit Mrna ◽  
Atpase Gene

Expression of the Na(+)-K(+)-adenosinetriphosphatase (ATPase) gene family in rat intestinal epithelial cells was examined using RNA blot hybridization analyses. Rat intestinal epithelial cells express only the alpha 1- and beta 1-subunit mRNAs. A gradient in expression of alpha 1- and beta 1-subunit mRNA was seen along the villus-crypt unit in both jejunum and ileum, i.e., villus tip >> crypt cells. Regional differences in expression were observed along the intestine. alpha 1- and beta 1-subunit mRNA abundance was similar in jejunum, ileum, and colon while enzymatic activity was highest in the jejunum and lowest in the ileum. Administration of thyroid hormone to thyroidectomized rats increased the expression of alpha 1- and beta 1-subunit mRNAs in jejunum but not in colon. Hypothyroidism had no effect on subunit mRNA expression. The human intestinal cell line Caco-2 was also studied. These cells also expressed only the alpha 1- and beta 1-isoform mRNAs and demonstrated a developmental profile in both mRNA and enzymatic activity. Furthermore, in Caco-2 cells both alpha 1- and beta 1-mRNAs and Na(+)-K(+)-ATPase enzymatic activity were stimulated by thyroid hormone. Caco-2 cells transfected with 5' flanking regions of the human Na(+)-K(+)-ATPase beta 1-gene linked to the chloramphenicol acetyltransferase (CAT) reporter gene responded to 3,5,3'-triiodothyronine (T3) treatment with increased expression of CAT activity. This suggests that the 5' flanking region of the beta 1-gene contains a thyroid hormone response element and that T3 upregulation occurs at the transcriptional level.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Post-Mortem Electrical Stimulation of Muscle and its Effects on Sarcoplasmic Reticulum Adenosine Triphosphatase

1979 ◽  
Vol 32 (2) ◽  
pp. 163 ◽  
Author(s):  
Ronald K Tume
Keyword(s):  
Electrical Stimulation ◽  
Sarcoplasmic Reticulum ◽  
Calcium Binding ◽  
Membrane Lipids ◽  
Protein A ◽  
Binding Affinities ◽  
Post Mortem ◽  
Short Term ◽  
Reduced Activity ◽  
Stimulation Of

Sarcoplasmic reticulum (SR) was isolated from control muscles and from muscles which had been subjected to short-term post-mortem electrical stimulation. Both preparations had similar protein compositions but the SR from electrically stimulated muscle had a lower 'extra' ATPase activity. The ability of the SR preparations from electrically stimulated muscles to accumulate Ca2+ was about the same as the controls. There was, therefore, an apparently greater efficiency of Ca2+ transport in the isolated vesicles, the reason for which is not known, but an alteration in the 'leakiness' of the membrane may be involved. Purified ATPase isolated from control and stimulated SR contained, in addition to the ATPase protein, a polypeptide of molecular weight about 30000. The purified ATPase vesicles from electrically stimulated muscle had a reduced activity as measured by ATP splitting activity, phosphoenzyme formation from either inorganic orthophosphate (Pi) or ATP, or by an ATP � Pi exchange reaction. These reduced activities probably result from an alteration in the binding affinities of the ATPase for ATP and Pi' The low affinity site for calcium binding was not affected by electrical stimulation. Purified ATPase vesicles from stimulated muscle were more susceptible to proteolytic attack, suggesting that the conformation of the protein or its association with the membrane lipids had been altered.

Thyroid hormone-induced stimulation of the sarcoplasmic reticulum Ca2+ ATPase gene is inhibited by LIF and IL-6

2000 ◽  
Vol 278 (4) ◽  
pp. E738-E743 ◽  
Author(s):  
Bernd Gloss ◽  
Sonia Villegas ◽  
Francisco J. Villarreal ◽  
Anselmo Moriscot ◽  
Wolfgang H. Dillmann
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Transcriptional Activity ◽  
Neonatal Rat ◽  
Mrna Levels ◽  
Cytokine Inhibition ◽  
Atpase Gene ◽  
Promoter Construct

We investigated the effects of the leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) on 3,3′, 5-triiodo-l-thyronine, or thyroid hormone (T3)-stimulated sarcoplasmic reticulum Ca2+ATPase (SERCA2) gene expression on cultured neonatal rat cardiac myocytes. A reduction of T3 induced increases in SERCA2 mRNA levels after co-treatment with LIF or IL-6. To investigate for the molecular mechanism(s) responsible for the blunted gene expression, a 3.2-kb SERCA2 promoter construct containing a reporter gene was transfected into cardiac myocytes. T3 treatment stimulated transcriptional activity twofold, whereas co-treatment with T3 and either of the cytokines caused an inhibition of T3-induced SERCA2 transcriptional activity. A T3-responsive 0.6-kb SERCA2 construct also showed a similar inhibition by cytokines. Cytokine inhibition of SERCA2 transcriptional activity was also evident when a 0.6-kb SERCA2 mutant, T3-unresponsive promoter construct was used. Treatment with T3 and cytokines showed a significant decrease in transcription when a reporter construct was used that was comprised of direct repeats of SERCA2 thyroid response element I. These data provide evidence for cytokine-mediated inhibitory effects on the SERCA2 promoter that may be mediated by interfering with T3action.

Observation of Velopharyngeal Closure Patterns following Isolated Stimulation of Levator Veli Palatini and Pharyngeal Constrictor Muscles

1996 ◽  
Vol 33 (4) ◽  
pp. 273-276 ◽  
Author(s):  
Mikihiko Kogo ◽  
Munehiro Hamaguchi ◽  
Tokuzo Matsuya
Keyword(s):  
Electrical Stimulation ◽  
Motor Nerve ◽  
Lateral Wall ◽  
Vertical Movement ◽  
Levator Veli Palatini ◽  
Velopharyngeal Closure ◽  
The Individual ◽  
Pharyngeal Constrictor Muscles ◽  
Peripheral Motor ◽  
Stimulation Of

This study, using mongrel dogs, showed the individual movements caused by the levator veli palatini muscle (LVP) and pharyngeal constrictor (PC) contraction, induced by electrical stimulation to each peripheral motor nerve. Each bilateral peripheral motor nerve of the LVP and PC muscles was isolated and stimulated electrically to induce the individual contraction of bilateral LVP and PC muscles. The movements were visualized by use of a fiberscope. Vertical movement of the middle soft palate was observed mainly at LVP contraction. Circular closure in the posterior region of the velopharynx was induced by contraction of the PC muscle. The posterior and lateral wall movements clearly occurred following PC contraction.

Mechanism of Thyroid-Hormone Regulated Expression of the SERCA Genes in Skeletal Muscle: Implications for Thermogenesis

2001 ◽  
Vol 21 (2) ◽  
pp. 139-154 ◽  
Author(s):  
Walter S. Simonides ◽  
Marc H. M. Thelen ◽  
C. Gerard van der Linden ◽  
Alice Muller ◽  
Cornelis van Hardeveld
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Atpase Activity ◽  
Contractile Activity ◽  
Slow Muscle ◽  
Hormone Response Elements ◽  
Serum T3 ◽  
Specific Stimulation ◽  
High Average Level ◽  
Stimulation Of

Thyroid hormone increases the Ca2+-ATPase activity of the sarcoplasmic reticulum (SR) in skeletal muscle, thereby increasing the energy-turnover associated with Ca2+-cycling during contraction and rest. The fast-muscle isoform of the Ca2+-ATPase (SERCA1) and the slow-muscle isoform (SERCA2a), are encoded by two genes that are transcriptionally regulated by T3. The SERCA1 isoform can be expressed to considerably higher levels than the SERCA2a isoform. The stimulation of transcription of the SERCA1 gene by T3 is mediated by two thyroid hormone response elements, located in the promoter of this gene. The intracellular [Ca2+] can modulate the effect of T3. The increase in SR Ca2+-ATPase activity seen when T3-levels rise above normal, results from the induction of SERCA1 expression in slow muscle fibers. Concomitant high levels of Ca2+-ATPase activity are associated with down-regulation of SERCA2a expression in these fibers. The observed T3-dependent increase in SERCA1 expression and associated Ca2+-ATPase activity will increase the overall metabolic rate of the organism significantly under normal conditions, because of the high average level of contractile activity of slow fibers. Given the rise in serum T3-levels during prolonged cold exposure, these data suggest that fiber-specific stimulation of SERCA1 expression contributes to the thermogenic response in non-shivering thermogenesis. This mechanism may be particularly relevant in larger mammals, which have a relatively high percentage of slow fibers in skeletal muscle, and which need to rely on tissues other than brown fat for the generation of extra heat.

scholarly journals Cross-talk between transcriptional regulation by thyroid hormone and myogenin: new aspects of the Ca2+-dependent expression of the fast-type sarcoplasmic reticulum Ca2+-ATPase

1998 ◽  
Vol 329 (1) ◽  
pp. 131-136 ◽  
Author(s):  
H. M. Marc THELEN ◽  
S. Warner SIMONIDES ◽  
Alice MULLER ◽  
Cornelis VAN HARDEVELD
Keyword(s):  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Transcriptional Regulation ◽  
Thyroid Hormone ◽  
Promoter Activity ◽  
Transcriptional Activity ◽  
Contractile Activity ◽  
L6 Cells ◽  
Translational Level ◽  
Stimulation Of

We have previously demonstrated an interaction between the major determinants of skeletal muscle phenotype by showing that continuous contractile activity represses the thyroid hormone (3,3ʹ,5-tri-iodothyronine; T3)-dependent transcriptional activity of fast-type sarcoplasmic/endoplasmic-reticulum Ca2+-ATPase (SERCA1), a characteristic of the fast phenotype. Both the free cytosolic Ca2+ concentration ([Ca2+]i) and the myogenic determination factors MyoD and myogenin have been implicated as mediators of the effect of contractile activity on skeletal muscle phenotype. Using L6 cells we have shown that an increase in the steady-state [Ca2+]i above the resting level of 120 nM indeed can mimic the effect of contractile activity on T3-dependent SERCA1 expression. We now show that the repressing effect of increased [Ca2+]i on T3-dependent SERCA1 expression in L6 cells is exerted at a pre-translational level and is accompanied by increased myogenin mRNA expression. Myogenin overexpression in these cells revealed that increased expression of myogenin alone strongly decreases the T3-dependent stimulation of SERCA1 promoter activity. These results suggest a pathway for the regulation of skeletal muscle phenotype in which [Ca2+]i mediates the effect of contractile activity by regulating the expression of myogenin, which in turn interferes with transcriptional regulation by T3.

scholarly journals KATP channels and NO dilate redundantly intramuscular arterioles during electrical stimulation of the skeletal muscle in mice

2021 ◽  
Author(s):  
Simon Schemke ◽  
Cor de Wit
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Motor Nerve ◽  
Neuromuscular Synapse ◽  
Katp Channels ◽  
Neuromuscular Synapses ◽  
Maximal Diameter ◽  
Motor Nerves ◽  
A Minor ◽  
Stimulation Of

AbstractFunctional hyperemia is fundamental to provide enhanced oxygen delivery during exercise in skeletal muscle. Different mechanisms are suggested to contribute, mediators from skeletal muscle, transmitter spillover from the neuromuscular synapse as well as endothelium-related dilators. We hypothesized that redundant mechanisms that invoke adenosine, endothelial autacoids, and KATP channels mediate the dilation of intramuscular arterioles in mice. Arterioles (maximal diameter: 20–42 µm, n = 65) were studied in the cremaster by intravital microscopy during electrical stimulation of the motor nerve to induce twitch or tetanic skeletal muscle contractions (10 or 100 Hz). Stimulation for 1–60 s dilated arterioles rapidly up to 65% of dilator capacity. Blockade of nicotinergic receptors blocked muscle contraction and arteriolar dilation. Exclusive blockade of adenosine receptors (1,3-dipropyl-8-(p-sulfophenyl)xanthine) or of NO and prostaglandins (nitro-L-arginine and indomethacin, LN + Indo) exerted only a minor attenuation. Combination of these blockers, however, reduced the dilation by roughly one-third during longer stimulation periods (> 1 s at 100 Hz). Blockade of KATP channels (glibenclamide) which strongly reduced adenosine-induced dilation reduced responses upon electrical stimulation only moderately. The attenuation was strongly enhanced if glibenclamide was combined with LN + Indo and even observed during brief stimulation. LN was more efficient than indomethacin to abrogate dilations if combined with glibenclamide. Arteriolar dilations induced by electrical stimulation of motor nerves require muscular contractions and are not elicited by acetylcholine spillover from neuromuscular synapses. The dilations are mediated by redundant mechanisms, mainly activation of KATP channels and release of NO. The contribution of K+ channels and hyperpolarization sets the stage for ascending dilations that are crucial for a coordinated response in the network.

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