Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT<sub>1</sub> receptor and NADPH oxidase

Cozzoli, Anna; Liantonio, Antonella; Conte, Elena; Cannone, Maria; Massari, Ada Maria; Giustino, Arcangela; Scaramuzzi, Antonia; Pierno, Sabata; Mantuano, Paola; Capogrosso, Roberta Francesca; Camerino, Claudia; A, De Luca

doi:10.1152/ajpcell.00372.2013

Cited by 31 publications

(32 citation statements)

References 82 publications

(178 reference statements)

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“…This hormone has been implicated in the pathology of conditions such as cardiac failure and kidney disease-related muscle atrophy (18). The relationship between AT II and NOX2 in skeletal muscle has been evaluated by different researchers (69,169). One study suggested using pharmacological inhibitors that AT II signals via NOX2 to increase intracellular Ca 2+ in mouse EDL skeletal muscle fibers (69).…”

Section: Fig 15 Nox2-dependent Omentioning

confidence: 99%

“…The relationship between AT II and NOX2 in skeletal muscle has been evaluated by different researchers (69,169). One study suggested using pharmacological inhibitors that AT II signals via NOX2 to increase intracellular Ca 2+ in mouse EDL skeletal muscle fibers (69). Experiments in vitro using C2C12 myotubes indicated that AT II increased the ROS production by a DPI-inhibitable NOX2-dependent mechanism (305).…”

Section: Fig 15 Nox2-dependent Omentioning

confidence: 99%

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The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Henríquez‐Olguín

Boronat

Cabello-Verrugio

et al. 2019

Antioxidants & Redox Signaling

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Significance: Skeletal muscle is a crucial tissue to whole-body locomotion and metabolic health. Reactive oxygen species (ROS) have emerged as intracellular messengers participating in both physiological and pathological adaptations in skeletal muscle. A complex interplay between ROS-producing enzymes and antioxidant networks exists in different subcellular compartments of mature skeletal muscle. Recent evidence suggests that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are a major source of contraction-and insulin-stimulated oxidants production, but they may paradoxically also contribute to muscle insulin resistance and atrophy. Recent Advances: Pharmacological and molecular biological tools, including redox-sensitive probes and transgenic mouse models, have generated novel insights into compartmentalized redox signaling and suggested that NOX2 contributes to redox control of skeletal muscle metabolism. Critical Issues: Major outstanding questions in skeletal muscle include where NOX2 activation occurs under different conditions in health and disease, how NOX2 activation is regulated, how superoxide/hydrogen peroxide generated by NOX2 reaches the cytosol, what the signaling mediators are downstream of NOX2, and the role of NOX2 for different physiological and pathophysiological processes. Future Directions: Future research should utilize and expand the current redox-signaling toolbox to clarify the NOX2-dependent mechanisms in skeletal muscle and determine whether the proposed functions of NOX2 in cells and animal models are conserved into humans.

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Section: Fig 15 Nox2-dependent Omentioning

confidence: 99%

Section: Fig 15 Nox2-dependent Omentioning

confidence: 99%

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

Henríquez‐Olguín

Boronat

Cabello-Verrugio

et al. 2019

Antioxidants & Redox Signaling

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“…Furthermore, electrophysiological studies showed an increase of gCl in the PKC𝜃-null mice with respect to wild-type, and a consequent reduction of muscle excitability ( Camerino et al, 2014 ). Regulation of ClC-1 channels through PKC-dependent phosphorylation appeared to be involved in the muscular effects of a number of growth factors, hormones, and drugs, including the growth hormone, insulin-like growth factor-1 (IGF-1), ghrelin, angiotensin II, growth hormone secretagogues, and statins ( De Luca et al, 1994b , 1998 ; Pierno et al, 2003 ; Cozzoli et al, 2014 ).…”

Section: Molecular Structure and Function Of Clc-1mentioning

confidence: 99%

ClC-1 chloride channels: state-of-the-art research and future challenges

Imbrici

Altamura

Pessia

et al. 2015

Front. Cell. Neurosci.

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The voltage-dependent ClC-1 chloride channel belongs to the CLC channel/transporter family. It is a homodimer comprising two individual pores which can operate independently or simultaneously according to two gating modes, the fast and the slow gate of the channel. ClC-1 is preferentially expressed in the skeletal muscle fibers where the presence of an efficient Cl- homeostasis is crucial for the correct membrane repolarization and propagation of action potential. As a consequence, mutations in the CLCN1 gene cause dominant and recessive forms of myotonia congenita (MC), a rare skeletal muscle channelopathy caused by abnormal membrane excitation, and clinically characterized by muscle stiffness and various degrees of transitory weakness. Elucidation of the mechanistic link between the genetic defects and the disease pathogenesis is still incomplete and, at this time, there is no specific treatment for MC. Still controversial is the subcellular localization pattern of ClC-1 channels in skeletal muscle as well as its modulation by some intracellular factors. The expression of ClC-1 in other tissues such as in brain and heart and the possible assembly of ClC-1/ClC-2 heterodimers further expand the physiological properties of ClC-1 and its involvement in diseases. A recent de novo CLCN1 truncation mutation in a patient with generalized epilepsy indeed postulates an unexpected role of this channel in the control of neuronal network excitability. This review summarizes the most relevant and state-of-the-art research on ClC-1 chloride channels physiology and associated diseases.

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“…, ; Cozzoli et al . ). A more physiological role of PKC‐dependent ClC‐1 inhibition was discovered when repeated firing of APs in rat muscle fibres were found to cause a more than 50% reduction in G m that was sensitive to PKC inhibition (Pedersen et al .…”

Section: Introductionmentioning

confidence: 97%

Protein kinase C‐dependent regulation of ClC‐1 channels in active human muscle and its effect on fast and slow gating

Riisager

Paoli

et al. 2016

The Journal of Physiology

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Key pointsr Regulation of ion channel function during repeated firing of action potentials is commonly observed in excitable cells. Recently it was shown that muscle activity is associated with rapid, protein kinase C (PKC)-dependent ClC-1 Cl − channel inhibition in rodent muscle.r While this PKC-dependent ClC-1 inhibition during muscle activity was shown to be important for the maintenance of contractile endurance in rat muscle it is unknown whether a similar regulation exists in human muscle.r Also, the molecular mechanisms underlying the observed PKC-dependent ClC-1 inhibition are unclear.r Here we present the first demonstration of ClC-1 inhibition in active human muscle fibres, and we determine the changes in ClC-1 gating that underlie the PKC-dependent ClC-1 inhibition in active muscle using human ClC-1 expressed in Xenopus oocytes.r This activity-induced ClC-1 inhibition is suggested to represent a mechanism by which human muscle fibres maintain their excitability during sustained activity.Abstract Repeated firing of action potentials (APs) is known to trigger rapid, protein kinase C (PKC)-dependent inhibition of ClC-1 Cl − ion channels in rodent muscle and this inhibition is important for contractile endurance. It is currently unknown whether similar regulation exists in human muscle, and the molecular mechanisms underlying PKC-dependent ClC-1 inhibition are unclear. This study first determined whether PKC-dependent ClC-1 inhibition exists in active human muscle, and second, it clarified how PKC alters the gating of human ClC-1 expressed in Xenopus oocytes. In human abdominal and intercostal muscles, repeated AP firing was associated with 30-60% reduction of ClC-1 function, which could be completely prevented by PKC inhibition (1 μM GF109203X). The role of the PKC-dependent ClC-1 inhibition was evaluated from rheobase currents before and after firing 1000 APs: while rheobase current was well maintained after activity under control conditions it rose dramatically if PKC-dependent ClC-1 inhibition had been prevented with the inhibitor. This demonstrates that the ClC-1 inhibition is important for maintenance of excitability in active human muscle fibres. Oocyte experiments showed that PKC activation lowered the overall open probability of ClC-1 in the voltage range relevant for AP initiation in muscle fibres. More detailed analysis of this reduction showed that PKC mostly affected the slow gate of ClC-1. Indeed, there was no effect of PKC activation in C277S mutated ClC-1 in which the slow gate is effectively locked open. It is concluded that regulation of excitability of active human muscle fibres relies on PKC-dependent ClC-1 inhibition via a gating mechanism.

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Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT₁ receptor and NADPH oxidase

Cited by 31 publications

References 82 publications

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

ClC-1 chloride channels: state-of-the-art research and future challenges

Protein kinase C‐dependent regulation of ClC‐1 channels in active human muscle and its effect on fast and slow gating

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Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT1 receptor and NADPH oxidase

Cited by 31 publications

References 82 publications

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism

ClC-1 chloride channels: state-of-the-art research and future challenges

Protein kinase C‐dependent regulation of ClC‐1 channels in active human muscle and its effect on fast and slow gating

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Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT₁ receptor and NADPH oxidase