Adaptive responses of TRPC1 and TRPC3 during skeletal muscle atrophy and regrowth

Zhang, Bao-Ting; Yeung, Simon S.; Cheung, Kwok-Kuen; Chai, Zacary Y.; Yeung, Ella W.

doi:10.1002/mus.23952

Cited by 28 publications

(25 citation statements)

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“…; Zhang et al . ) and establish the process by which skeletal muscles adapt to changes in mechanical stimuli.…”

Section: Resultsmentioning

confidence: 99%

“…; Zhang et al . ). Briefly, orthopaedic traction tape was applied to the animal from the end of the tail to around two‐thirds of the tail proximally.…”

Section: Methodsmentioning

confidence: 97%

“…Furthermore, TRPC1 expression was not upregulated until the later stages of reloading (Zhang et al . ). Thus, our working hypothesis is that downregulation of TRPC1 may impair the recovery of muscle mass during regrowth following atrophy.…”

Section: Introductionmentioning

confidence: 97%

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The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading‐induced atrophy

Xia

Cheung

Yeung

et al. 2016

The Journal of Physiology

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Key pointsr Decreased mechanical loading results in skeletal muscle atrophy. The transient receptor potential canonical type 1 (TRPC1) protein is implicated in this process. Investigation of the regulation of TRPC1 in vivo has rarely been reported. In the present study, we employ the mouse hindlimb unloading and reloading model to examine the involvement of TRPC1 in the regulation of muscle atrophy and regrowth, respectively.r We establish the physiological relevance of the concept that manipulation of TRPC1 could interfere with muscle regrowth processes following an atrophy-inducing event. Specifically, we show that suppressing TRPC1 expression during reloading impairs the recovery of the muscle mass and slow myosin heavy chain profile. Calcineurin appears to be part of the signalling pathway involved in the regulation of TRPC1 expression during muscle regrowth.r These results provide new insights concerning the function of TRPC1. Interventions targeting TRPC1 or its downstream or upstream pathways could be useful for promoting muscle regeneration.Abstract Decreased mechanical loading, such as bed rest, results in skeletal muscle atrophy. The functional consequences of decreased mechanical loading include a loss of muscle mass and decreased muscle strength, particularly in anti-gravity muscles. The purpose of this investigation was to clarify the regulatory role of the transient receptor potential canonical type 1 (TRPC1) protein during muscle atrophy and regrowth. Mice were subjected to 14 days of hindlimb unloading followed by 3, 7, 14 and 28 days of reloading. Weight-bearing mice were used as controls. TRPC1 expression in the soleus muscle decreased significantly and persisted at 7 days of reloading. Small interfering RNA (siRNA)-mediated downregulation of TRPC1 in weight-bearing soleus muscles resulted in a reduced muscle mass and a reduced myofibre cross-sectional area (CSA). Microinjecting siRNA into soleus muscles in vivo after 7 days of reloading provided further evidence for the role of TRPC1 in regulating muscle regrowth. Myofibre CSA, as well as the percentage of slow myosin heavy chain-positive myofibres, was significantly lower in TRPC1-siRNA-expressing muscles than in control muscles after 14 days of reloading. Additionally, inhibition of calcineurin (CaN) activity downregulated TRPC1 expression in both weight-bearing and reloaded muscles, suggesting a possible association between CaN and TRPC1 during skeletal muscle regrowth.

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“…; Zhang et al . ) and establish the process by which skeletal muscles adapt to changes in mechanical stimuli.…”

Section: Resultsmentioning

confidence: 99%

“…; Zhang et al . ). Briefly, orthopaedic traction tape was applied to the animal from the end of the tail to around two‐thirds of the tail proximally.…”

Section: Methodsmentioning

confidence: 97%

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The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading‐induced atrophy

Xia

Cheung

Yeung

et al. 2016

The Journal of Physiology

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“…TRPC1 also participates in an adaptive response of skeletal muscle (i.e., muscle regeneration). Down-regulation of TRPC1 expression is required for the regrowth of the mouse soleus muscle after muscle atrophy and the inhibition of calcineurin (CaN) signaling is involved in the down-regulation of TRPC1 expression [122,123]. Additionally, the PI 3 K/Akt/p70S6K pathway plays an important role in muscle regeneration and development and Ca 2+ entry through TRPC1 has been shown to play a role in the activation of the PI 3 K/Akt/p70S6K pathway during the regenerating of TA and EDL muscles [124].…”

Section: Trpc1 and Trpc4 In Skeletal Musclementioning

confidence: 99%

“…Concerning a model where TRPC3 is knocked down with siRNA in α1DHPR-null mouse skeletal myoblasts, there are severe defects in the proliferation of myoblasts and apoptosis during the terminal differentiation, suggesting that the coordinated Ca 2+ entry through both TRPC3 and DHPR is important for the terminal differentiation process [129]. Interestingly, like TRPC1, TRPC3 expression is down-regulated during the early phase of regrowth of mouse hind limb muscle after atrophy [123]. TRPC3 has been shown to form heteromers with TRPC1 via its ankyrin repeats and regulates the resting cytosolic Ca 2+ levels in mouse skeletal myotubes [130].…”

Section: Trpc3 and Trpc6 In Skeletal Musclementioning

confidence: 99%

TRPCs: Influential Mediators in Skeletal Muscle

Choi

Jeong

et al. 2020

Cells

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Ca 2+ itself or Ca 2+ -dependent signaling pathways play fundamental roles in various cellular processes from cell growth to death. The most representative example can be found in skeletal muscle cells where a well-timed and adequate supply of Ca 2+ is required for coordinated Ca 2+ -dependent skeletal muscle functions, such as the interactions of contractile proteins during contraction. Intracellular Ca 2+ movements between the cytosol and sarcoplasmic reticulum (SR) are strictly regulated to maintain the appropriate Ca 2+ supply in skeletal muscle cells. Added to intracellular Ca 2+ movements, the contribution of extracellular Ca 2+ entry to skeletal muscle functions and its significance have been continuously studied since the early 1990s. Here, studies on the roles of channel proteins that mediate extracellular Ca 2+ entry into skeletal muscle cells using skeletal myoblasts, myotubes, fibers, tissue, or skeletal muscle-originated cell lines are reviewed with special attention to the proposed functions of transient receptor potential canonical proteins (TRPCs) as store-operated Ca 2+ entry (SOCE) channels under normal conditions and the potential abnormal properties of TRPCs in muscle diseases such as Duchenne muscular dystrophy (DMD).

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Mechanosensing in Metabolism

Tranter,

Kumar,

Nair

et al. 2023

Comprehensive Physiology

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Electrical mechanosensing is a process mediated by specialized ion channels, gated directly or indirectly by mechanical forces, which allows cells to detect and subsequently respond to mechanical stimuli. The activation of mechanosensitive (MS) ion channels, intrinsically gated by mechanical forces, or mechanoresponsive (MR) ion channels, indirectly gated by mechanical forces, results in electrical signaling across lipid bilayers, such as the plasma membrane. While the functions of mechanically gated channels within a sensory context (e.g., proprioception and touch) are well described, there is emerging data demonstrating functions beyond touch and proprioception, including mechanoregulation of intracellular signaling and cellular/systemic metabolism. Both MR and MS ion channel signaling have been shown to contribute to the regulation of metabolic dysfunction, including obesity, insulin resistance, impaired insulin secretion, and inflammation. This review summarizes our current understanding of the contributions of several MS/MR ion channels in cell types implicated in metabolic dysfunction, namely, adipocytes, pancreatic β‐cells, hepatocytes, and skeletal muscle cells, and discusses MS/MR ion channels as possible therapeutic targets. © 2024 American Physiological Society. Compr Physiol 14:5269‐5290, 2024.

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Adaptive responses of TRPC1 and TRPC3 during skeletal muscle atrophy and regrowth

Abstract: Given the known role of these channels in muscle development, changes observed in TRPC1 and TRPC3 may relate closely to muscle atrophy and remodeling processes.

Cited by 28 publications

References 50 publications

The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading‐induced atrophy

The involvement of transient receptor potential canonical type 1 in skeletal muscle regrowth after unloading‐induced atrophy

TRPCs: Influential Mediators in Skeletal Muscle

Mechanosensing in Metabolism

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