Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force

Hinkle, Richard T.; Donnelly, Elizabeth; Cody, David B.; Sheldon, Russell J.; Isfort, Robert J.

doi:10.1152/japplphysiol.00736.2004

Cited by 15 publications

(15 citation statements)

References 45 publications

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“…Unlike PACAP knockout animals, mice with targeted VIP gene disruption displayed subtle but significant reductions in muscular strength as revealed in the grip strength and wire maneuver tasks. These results appear consistent with recent studies demonstrating that VIP and VPAC2 receptor signaling play key roles in the physiological control of skeletal muscle mass and ameliorating muscle loss from atrophic conditions (Hinkle et al . 2005).…”

Section: Discussionsupporting

confidence: 93%

Noncompensation in peptide/receptor gene expression and distinct behavioral phenotypes in VIP‐ and PACAP‐deficient mice

Girard

Lelièvre

Braas

et al. 2006

Journal of Neurochemistry

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Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are closely related neurotrophic peptides of the secretin/glucagon family. The two peptides are derived from a common ancestral gene and share many functional attributes in neuronal development/ regeneration which occur not only from overlapping receptor subtype signaling but also through common mechanisms regulating their expression. Although PACAP or VIP null mice have been generated for study, it is unclear whether the expression of the complementary peptide or their receptor systems are altered in a compensatory manner during nervous system development. By radioimmunoassay and quantitative PCR measurements, we first show that PACAP and VIP have very different temporal patterns of expression in developing postnatal mouse brain. In wild-type animals, PA-CAP transcript and peptide levels increased rapidly 2-and 5-fold, respectively, within 1 week of age. These levels at 1 week of age were maintained through adulthood. VIP transcript and peptide levels, by contrast, increased 25-and 50-fold, respectively, over a later time course. In parallel studies of development, there were no apparent compensatory increases in brain VIP expression in the PACAP knockout animals, PACAP expression in the VIP-deficient animals, or receptor mRNA levels in either genotype. To the contrary, there was evidence for developmental delays in the expression of peptide and receptor transcripts in the knockout animals. A series of behavioral and neurological tests demonstrated differences between the knockout genotypes, revealing some functional distinctions between the two genes. These results suggest that the PACAP and VIP have evolved to possess distinct biological activities and intimate that the respective knockout phenotypes represent deficits unmitigated by the actions of the complementary related peptide. Abbreviations : cDNA, complementary DNA; CGRP, calcitonin generelated peptide; PAC 1 , PACAP-selective G-protein-coupled receptor; PACAP, pituitary adenylate cyclase-activating polypeptide; R n , normalized reporter of quantitative PCR equal to the ratio of the fluorescence emission of the reporter dye, SYBR Green I, and the internal reference dye; DR n , signal magnitude determined as the difference between the R n value of the sample containing all of the reaction components and that determined under no template control conditions; SHIRPA, (SmithKline

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Section: Discussionsupporting

confidence: 93%

Noncompensation in peptide/receptor gene expression and distinct behavioral phenotypes in VIP‐ and PACAP‐deficient mice

Girard

Lelièvre

Braas

et al. 2006

Journal of Neurochemistry

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“…Evaluation of muscle cAMP levels was performed as described by us previously [32,33]. Briefly, skeletal muscle tissue baths were prepared by dissecting the medial gastrocnemius and tibialis anterior muscles from both the right and left legs of mice and pinning the muscles at resting length on rubber supports adhered to glass microscope slides.…”

Section: Methodsmentioning

confidence: 99%

“…Lower leg casting disuse-induced muscle atrophy was performed as described previously [32,33]. Briefly, mice were anesthetized with isoflurane and the lower right leg was casted from the knee to the toes with heat activated casting material (Vet Lite, Kruuse Inc., Marslev, Denmark).…”

Section: Methodsmentioning

confidence: 99%

Activation of the dopamine 1 and dopamine 5 receptors increase skeletal muscle mass and force production under non-atrophying and atrophying conditions

Reichart

Hinkle

Lefever

et al. 2011

BMC Musculoskelet Disord

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BackgroundControl of skeletal muscle mass and force production is a complex physiological process involving numerous regulatory systems. Agents that increase skeletal muscle cAMP levels have been shown to modulate skeletal muscle mass and force production. The dopamine 1 receptor and its closely related homolog, the dopamine 5 receptor, are G-protein coupled receptors that are expressed in skeletal muscle and increase cAMP levels when activated. Thus we hypothesize that activation of the dopamine 1 and/or 5 receptor will increase skeletal muscle cAMP levels thereby modulating skeletal muscle mass and force production.MethodsWe treated isolated mouse tibialis anterior (TA) and medial gastrocnemius (MG) muscles in tissue bath with the selective dopamine 1 receptor and dopamine 5 receptor agonist SKF 81297 to determine if activation of skeletal muscle dopamine 1 and dopamine 5 receptors will increase cAMP. We dosed wild-type mice, dopamine 1 receptor knockout mice and dopamine 5 receptor knockout mice undergoing casting-induced disuse atrophy with SKF 81297 to determine if activation of the dopamine 1 and dopamine 5 receptors results in hypertrophy of non-atrophying skeletal muscle and preservation of atrophying skeletal muscle mass and force production.ResultsIn tissue bath, isolated mouse TA and MG muscles responded to SKF 81297 treatment with increased cAMP levels. Treating wild-type mice with SKF 81297 reduced casting-induced TA and MG muscle mass loss in addition to increasing the mass of non-atrophying TA and MG muscles. In dopamine 1 receptor knockout mice, extensor digitorum longus (EDL) and soleus muscle mass and force was not preserved during casting with SKF 81297 treatment, in contrast to significant preservation of casted wild-type mouse EDL and soleus mass and EDL force with SKF 81297 treatment. Dosing dopamine 5 receptor knockout mice with SKF 81297 did not significantly preserve EDL and soleus muscle mass and force although wild-type mouse EDL mass and force was significantly preserved SKF 81297 treatment.ConclusionsThese data demonstrate for the first time that treatment with a dopamine 1/5 receptor agonist results in (1) significant preservation of EDL, TA, MG and soleus muscle mass and EDL muscle force production during periods of atrophy and (2) hypertrophy of TA and MG muscle. These effects appear to be mainly mediated by both the dopamine 1 and dopamine 5 receptors.

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“…They were not fasted at the time of sacrifice. The left and right masseter muscles were each excised and weighed; muscle mass was used as an index of muscle growth (23,24). The central portion of the left superficial masseter muscle was divided into two pieces, which were rapidly frozen in liquid nitrogen and stored at −85°C for real-time quantitative PCR and SDS-PAGE analysis.…”

Section: −1mentioning

confidence: 99%

Effects of Chronic Akt/mTOR Inhibition by Rapamycin on Mechanical Overload–Induced Hypertrophy and Myosin Heavy Chain Transition in Masseter Muscle

et al. 2013

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Abstract.To examine the effects of the Akt/mammalian target of rapamycin (mTOR) pathway on masseter muscle hypertrophy and myosin heavy chain (MHC) transition in response to mechanical overload, we analyzed the effects of bite-opening (BO) on the hypertrophy and MHC composition of masseter muscle of BO-rats treated or not treated with rapamycin (RAPA), a selective mTOR inhibitor. The masseter muscle weight in BO-rats was significantly greater than that in controls, and this increase was attenuated by RAPA treatment. Expression of slow-twitch MHC isoforms was significantly increased in BO-rats with/without RAPA treatment, compared with controls, but the magnitude of the increase was much smaller in RAPA-treated BO-rats. Phosphorylation of p44/42 MAPK (ERK1/2), which preserves fast-twitch MHC isoforms in skeletal muscle, was significantly decreased in BO-rats, but the decrease was abrogated by RAPA treatment. Calcineurin signaling is known to be important for masseter muscle hypertrophy and fast-to-slow MHC isoform transition, but expression of known calcineurin activity modulators was unaffected by RAPA treatment. Taken together, these results indicate that the Akt/mTOR pathway is involved in both development of masseter muscle hypertrophy and fast-to-slow MHC isoform transition in response to mechanical overload with inhibition of the ERK1/2 pathway and operates independently of the calcineurin pathway.

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Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force

Abstract: . Activation of the vasoactive intestinal peptide 2 receptor modulates normal and atrophying skeletal muscle mass and force.

Cited by 15 publications

References 45 publications

Noncompensation in peptide/receptor gene expression and distinct behavioral phenotypes in VIP‐ and PACAP‐deficient mice

Noncompensation in peptide/receptor gene expression and distinct behavioral phenotypes in VIP‐ and PACAP‐deficient mice

Activation of the dopamine 1 and dopamine 5 receptors increase skeletal muscle mass and force production under non-atrophying and atrophying conditions

Effects of Chronic Akt/mTOR Inhibition by Rapamycin on Mechanical Overload–Induced Hypertrophy and Myosin Heavy Chain Transition in Masseter Muscle

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