Mitochondrial Calcium Oscillations in C2C12 Myotubes

Challet, Corinne; Maechler, Pierre; Wollheim, Claes B.; Rüegg, Urs T.

doi:10.1074/jbc.m006209200

Cited by 23 publications

(19 citation statements)

References 41 publications

(44 reference statements)

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“…Culture of C2C12 myotubes was performed as previously described (Schmitz-Peiffer et al, 1999;Challet et al, 2001). Mice C2C12 myoblasts were maintained in DMEM, at pH 7.4, containing 4.5 mg/ml glucose, 10% FCS, and penicillin/streptomycin (500 U/ml each), with 95% O 2 /5% CO 2 , at 378C.…”

Section: Culture Of Skeletal Muscle Cellsmentioning

confidence: 99%

Saturated fatty acid‐induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells

Hirabara

Curi

Maechler

2009

Journal Cellular Physiology

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178

124

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Increased plasma levels of free fatty acids (FFA) occur in states of insulin resistance such as obesity and type 2 diabetes mellitus. These high levels of plasma FFA are proposed to play an important role for the development of insulin resistance but the mechanisms involved are still unclear. This study investigated the effects of saturated and unsaturated FFA on insulin sensitivity in parallel with mitochondrial function. C2C12 myotubes were treated for 24 h with 0.1 mM of saturated (palmitic and stearic) and unsaturated (oleic, linoleic, eicosapentaenoic, and docosahexaenoic) FFA. After this period, basal and insulin-stimulated glucose metabolism and mitochondrial function were evaluated. Saturated palmitic and stearic acids decreased insulin-induced glycogen synthesis, glucose oxidation, and lactate production. Basal glucose oxidation was also reduced. Palmitic and stearic acids impaired mitochondrial function as demonstrated by decrease of both mitochondrial hyperpolarization and ATP generation. These FFA also decreased Akt activation by insulin. As opposed to saturated FFA, unsaturated FFA did not impair glucose metabolism and mitochondrial function. Primary cultures of rat skeletal muscle cells exhibited similar responses to saturated FFA as compared to C2C12 cells. These results show that in muscle cells saturated FFA-induced mitochondrial dysfunction associated with impaired insulin-induced glucose metabolism.

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Section: Culture Of Skeletal Muscle Cellsmentioning

confidence: 99%

Saturated fatty acid‐induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells

Hirabara

Curi

Maechler

2009

Journal Cellular Physiology

Self Cite

178

124

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“…Nonetheless, direct measurements of mitochondrial calcium using targeted calcium probes have demonstrated that mitochondria sequester calcium during cytoplasmic calcium oscillations in fibroblasts, endothelial/epithelial cells, cardiac/skeletal muscle cells, neurons, and pancreatic acinar cells 56. Efficient mitochondrial Ca 2+ uptake by the low‐affinity uniporter is explained by the presence of tight SR–mitochondria colocalization135 and the formation of functional calcium microdomains in skeletal muscle 36, 149…”

Section: Calcium Reuptakementioning

confidence: 99%

Sarcoplasmic reticulum: The dynamic calcium governor of muscle

2006

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The sarcoplasmic reticulum (SR) provides feedback control required to balance the processes of calcium storage, release, and reuptake in skeletal muscle. This balance is achieved through the concerted action of three major classes of SR calcium-regulatory proteins: (1) luminal calcium-binding proteins (calsequestrin, histidine-rich calcium-binding protein, junctate, and sarcalumenin) for calcium storage; (2) SR calcium release channels (type 1 ryanodine receptor or RyR1 and IP3 receptors) for calcium release; and (3) sarco(endo)plasmic reticulum Ca2+ -ATPase (SERCA) pumps for calcium reuptake. Proper calcium storage, release, and reuptake are essential for normal skeletal muscle function. We review SR structure and function during normal skeletal muscle activity, the proteins that orchestrate calcium storage, release, and reuptake, and how phenotypically distinct muscle diseases (e.g., malignant hyperthermia, central core disease, and Brody disease) can result from subtle alterations in the activity of several key components of the SR calcium-regulatory machinery.

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“…In excitable cells, the oscillation may depend on oscillatory Ca 2+ release through ryanodine receptors from the ER [11]. In nonexcitable cells, Ca 2+ oscillation is generated by sequential regenerative discharges of stored calcium for which most often (but not always) the bell-shaped Ca 2+ dependency of IP3Rs [4,6,25,33] is the basic mechanism.…”

Section: Mitochondrial Function and Cytosolic Ca 2+ Oscillationmentioning

confidence: 99%

“…The decay of the signal may be due to desensitisation of the mitochondrial Ca 2+ transport system, described, e.g. in pancreatic beta cells [41], in myotubes [11], in RBL-1 cells [49] and in HeLa cells [12,57]. In hepatocytes, cytosolic Ca 2+ oscillation is reliably transferred into the mitochondrial matrix, but sustained elevation of [Ca 2+ ] c evokes only transient increase in [Ca 2+ ] m and mitochondrial NAD(P)H [30,63].…”

Section: Generation Of Sustained Mitochondrial Ca 2+ and Nad (P)h Signalmentioning

confidence: 99%

Special features of mitochondrial Ca2+ signalling in adrenal glomerulosa cells

Spät

Szanda

2012

Pflugers Arch - Eur J Physiol

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Aldosterone, secreted by adrenal glomerulosa cells, allows the adaptation of the vertebrate organism to a wide range of physiological and pathological stimuli including acute haemodynamic challenges and long-term changes in dietary sodium and potassium intake. Most of the extracellular signals are mediated by cytosolic Ca²⁺ signal deriving from Ca²⁺ release, store-operated and/or voltage-gated Ca²⁺ influx. Mitochondria in glomerulosa cells play a fundamental role in generating and modulating the final biological response. These organelles not only house several enzymes of aldosterone biosynthesis but also-in a Ca²⁺-dependent manner-provide NADPH for the function of these enzymes. Moreover, mitochondria, constituting a high portion of cytoplasmic volume and displaying a uniquely low-threshold Ca²⁺ sequestering ability, shape and thus modulate the decoding of the complex cytosolic Ca²⁺ response. The unusual features of mitochondrial Ca²⁺ signalling that permit such an integrative function in adrenal glomerulosa cells are hereby described.

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Mitochondrial Calcium Oscillations in C2C12 Myotubes

Abstract: Mitochondrial

Cited by 23 publications

References 41 publications

Saturated fatty acid‐induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells

Saturated fatty acid‐induced insulin resistance is associated with mitochondrial dysfunction in skeletal muscle cells

Sarcoplasmic reticulum: The dynamic calcium governor of muscle

Special features of mitochondrial Ca2+ signalling in adrenal glomerulosa cells

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