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Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy

Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy
Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy
Objective: the Vitamin D receptor (VDR) has been positively associated with skeletal muscle mass, function and regeneration. Mechanistic studies have focused on the loss of the receptor, with in vivo whole-body knockout models demonstrating reduced myofibre size and function and impaired muscle development. To understand the mechanistic role upregulation of the VDR elicits in muscle mass/health, we studied the impact of VDR over-expression (OE) in vivo before exploring the importance of VDR expression upon muscle hypertrophy in humans.
Methods: wistar rats underwent in vivo electrotransfer (IVE) to overexpress the VDR in the Tibialis anterior (TA) muscle for 10 days, before comprehensive physiological and metabolic profiling to characterise the influence of VDR-OE on muscle protein synthesis (MPS), anabolic signalling and satellite cell activity. Stable isotope tracer (D2O) techniques were used to assess sub-fraction protein synthesis, alongside RNA-Seq analysis. Finally, human participants underwent 20 wks of resistance exercise training, with body composition and transcriptomic analysis.
Results: muscle VDR-OE yielded total protein and RNA accretion, manifesting in increased myofibre area, i.e., hypertrophy. The observed increases in MPS were associated with enhanced anabolic signalling, reflecting translational efficiency (e.g., mammalian target of rapamycin (mTOR-signalling), with no effects upon protein breakdown markers being observed. Additionally, RNA-Seq illustrated marked extracellular matrix (ECM) remodelling, while satellite cell content, markers of proliferation and associated cell-cycled related gene-sets were upregulated. Finally, induction of VDR mRNA correlated with muscle hypertrophy in humans following long-term resistance exercise type training.
Conclusion: VDR-OE stimulates muscle hypertrophy ostensibly via heightened protein synthesis, translational efficiency, ribosomal expansion and upregulation of ECM remodelling-related gene-sets. Furthermore, VDR expression is a robust marker of the hypertrophic response to resistance exercise in humans. The VDR is a viable target of muscle maintenance through testable Vitamin D molecules, as active molecules and analogues.
Bass, Joseph J.
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Nakhuda, Asif
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Deane, Colleen S.
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Brook, Mathew S.
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Wilkinson, Daniel J.
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Phillips, Bethan E.
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Philp, Andrew
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Tarum, Janelle
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Kadi, Fawzi
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Andersen, Ditte
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Garcia, Amadeo Munoz
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Smith, Ken
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Gallagher, Iain James
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Szewczyk, Nathaniel
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Cleasby, Mark E.
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Atherton, Philip J.
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Bass, Joseph J.
e93cd462-0593-4ef4-9088-c23cf42ef1e5
Nakhuda, Asif
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Deane, Colleen S.
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Brook, Mathew S.
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Wilkinson, Daniel J.
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Phillips, Bethan E.
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Philp, Andrew
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Tarum, Janelle
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Kadi, Fawzi
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Andersen, Ditte
9b275266-aaa9-402d-9922-8f5eaafb3be6
Garcia, Amadeo Munoz
20a00855-1f0c-4235-9d76-f36c57f76b6e
Smith, Ken
530b07c4-f3f4-4d82-90a7-ecffc73ad498
Gallagher, Iain James
dc144e9d-d0da-473f-b0c4-371a60246321
Szewczyk, Nathaniel
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Cleasby, Mark E.
5bcf5c05-556a-4045-9ac1-b335e65c45a2
Atherton, Philip J.
7862070e-c551-46c4-be02-cd9fb4344a5e

Bass, Joseph J., Nakhuda, Asif, Deane, Colleen S., Brook, Mathew S., Wilkinson, Daniel J., Phillips, Bethan E., Philp, Andrew, Tarum, Janelle, Kadi, Fawzi, Andersen, Ditte, Garcia, Amadeo Munoz, Smith, Ken, Gallagher, Iain James, Szewczyk, Nathaniel, Cleasby, Mark E. and Atherton, Philip J. (2020) Overexpression of the vitamin D receptor (VDR) induces skeletal muscle hypertrophy. Molecular Metabolism, 42, [101059]. (doi:10.1016/j.molmet.2020.101059).

Record type: Article

Abstract

Objective: the Vitamin D receptor (VDR) has been positively associated with skeletal muscle mass, function and regeneration. Mechanistic studies have focused on the loss of the receptor, with in vivo whole-body knockout models demonstrating reduced myofibre size and function and impaired muscle development. To understand the mechanistic role upregulation of the VDR elicits in muscle mass/health, we studied the impact of VDR over-expression (OE) in vivo before exploring the importance of VDR expression upon muscle hypertrophy in humans.
Methods: wistar rats underwent in vivo electrotransfer (IVE) to overexpress the VDR in the Tibialis anterior (TA) muscle for 10 days, before comprehensive physiological and metabolic profiling to characterise the influence of VDR-OE on muscle protein synthesis (MPS), anabolic signalling and satellite cell activity. Stable isotope tracer (D2O) techniques were used to assess sub-fraction protein synthesis, alongside RNA-Seq analysis. Finally, human participants underwent 20 wks of resistance exercise training, with body composition and transcriptomic analysis.
Results: muscle VDR-OE yielded total protein and RNA accretion, manifesting in increased myofibre area, i.e., hypertrophy. The observed increases in MPS were associated with enhanced anabolic signalling, reflecting translational efficiency (e.g., mammalian target of rapamycin (mTOR-signalling), with no effects upon protein breakdown markers being observed. Additionally, RNA-Seq illustrated marked extracellular matrix (ECM) remodelling, while satellite cell content, markers of proliferation and associated cell-cycled related gene-sets were upregulated. Finally, induction of VDR mRNA correlated with muscle hypertrophy in humans following long-term resistance exercise type training.
Conclusion: VDR-OE stimulates muscle hypertrophy ostensibly via heightened protein synthesis, translational efficiency, ribosomal expansion and upregulation of ECM remodelling-related gene-sets. Furthermore, VDR expression is a robust marker of the hypertrophic response to resistance exercise in humans. The VDR is a viable target of muscle maintenance through testable Vitamin D molecules, as active molecules and analogues.

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Accepted/In Press date: 28 July 2020
e-pub ahead of print date: 7 August 2020
Published date: 30 August 2020

Identifiers

Local EPrints ID: 483352
URI: http://eprints.soton.ac.uk/id/eprint/483352
PURE UUID: f789b745-c2f0-48a3-93b6-7d6333bf18e4
ORCID for Colleen S. Deane: ORCID iD orcid.org/0000-0002-2281-6479

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Date deposited: 30 Oct 2023 07:58
Last modified: 17 Mar 2024 04:15

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Contributors

Author: Joseph J. Bass
Author: Asif Nakhuda
Author: Colleen S. Deane ORCID iD
Author: Mathew S. Brook
Author: Daniel J. Wilkinson
Author: Bethan E. Phillips
Author: Andrew Philp
Author: Janelle Tarum
Author: Fawzi Kadi
Author: Ditte Andersen
Author: Amadeo Munoz Garcia
Author: Ken Smith
Author: Iain James Gallagher
Author: Nathaniel Szewczyk
Author: Mark E. Cleasby
Author: Philip J. Atherton

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