Neuregulin 1 improves complex 2-mediated mitochondrial respiration in skeletal muscle of healthy and diabetic mice

Ennequin, Gaël; Capel, Frédéric; Caillaud, Kévin; Chavanelle, Vivien; Etienne, Monique; Teixeira, Allison; Li, Xinyan; Sirvent, Pascal

doi:10.1038/s41598-017-02029-z

Cited by 20 publications

(19 citation statements)

References 55 publications

(54 reference statements)

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“…NRG1 regulates myogenesis 9 , muscle spindle development and maintenance 10 , glucose transport 11 , 12 , mitochondrial oxidative capacity 13 , 14 and acetylcholine receptor expression 8 , 15 . A role of the NRG1/ErbB system in muscle regeneration has been postulated, and NRG1 expression increases in satellite cells and motoneurons after toxin-induced muscle damage 16 .…”

Section: Introductionmentioning

confidence: 99%

Modulation of the Neuregulin 1/ErbB system after skeletal muscle denervation and reinnervation

Morano

Ronchi

Nicolò

et al. 2018

Sci Rep

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Neuregulin 1 (NRG1) is a growth factor produced by both peripheral nerves and skeletal muscle. In muscle, it regulates neuromuscular junction gene expression, acetylcholine receptor number, muscle homeostasis and satellite cell survival. NRG1 signalling is mediated by the tyrosine kinase receptors ErbB3 and ErbB4 and their co-receptors ErbB1 and ErbB2. The NRG1/ErbB system is well studied in nerve tissue after injury, but little is known about this system in skeletal muscle after denervation/reinnervation processes. Here, we performed a detailed time-course expression analysis of several NRG1 isoforms and ErbB receptors in the rat superficial digitorum flexor muscle after three types of median nerve injuries of different severities. We found that ErbB receptor expression was correlated with the innervated state of the muscle, with upregulation of ErbB2 clearly associated with the denervation state. Interestingly, the NRG1 isoforms were differently regulated depending on the nerve injury type, leading to the hypothesis that both the NRG1α and NRG1β isoforms play a key role in the muscle reaction to injury. Indeed, in vitro experiments with C2C12 atrophic myotubes revealed that both NRG1α and NRG1β treatment influences the best-known atrophic pathways, suggesting that NRG1 might play an anti-atrophic role.

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Section: Introductionmentioning

confidence: 99%

Modulation of the Neuregulin 1/ErbB system after skeletal muscle denervation and reinnervation

Morano

Ronchi

Nicolò

et al. 2018

Sci Rep

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“…Previous studies revealed, NRG1/ErbB pathway is impaired in DCM cells which suggested NRG1/ErbB pathway may play an important role in DCM (30)(31)(32). Besides, NRG1/ErbB can improve glucose tolerance in healthy and diabetic rodents (32). And, also previous studies showed NRG1 can regulate myocyte oxidative capacity (33,34).…”

Section: Discussionmentioning

confidence: 96%

“…Therefore, inhibiting oxidative stress is believed to be an important strategy for the therapy of DCM. Previous studies revealed, NRG1/ErbB pathway is impaired in DCM cells which suggested NRG1/ErbB pathway may play an important role in DCM (30)(31)(32). Besides, NRG1/ErbB can improve glucose tolerance in healthy and diabetic rodents (32).…”

Section: Discussionmentioning

confidence: 99%

<i>Astraglaus polysaccharide</i> protects diabetic cardiomyopathy by activating NRG1/ErbB pathway

Chang

Wang

et al. 2018

BST

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Diabetic cardiomyopathy (DCM) is one of the main cardiac complications among diabetic patients. According to previous studies, the pathogenesis of DCM is associated with oxidative stress, apoptosis and proliferation of local cardiac cells. It showed, NRG1 can improve the function of mitochondria, and thereby, increasing proliferation and decreasing apoptosis of cardiac muscle cell via ErbB/AKT signaling, also, exert antioxidative function. Besides, NRG1/ErbB pathway was impaired in the DCM model which suggested this signaling played key role in DCM. Astraglaus polysaccharide (APS), one of the active components of Astragalus mongholicus, showed striking antioxidative effect. Here, in this study, our data showed that APS can promote proliferation and decrease apoptosis in AGE-induced DCM cell model, besides, APS can decrease intracellular ROS level, increase activity of SOD, GSH-Px and lower level of MDA and NO in DCM cell model, indicating APS exerted antioxidative function in DCM model cells. Besides, western blot results revealed APS induced NRG1 expressing and the phosphorylation level of ErbB2/4. In addition, the elevated NRG1 promoted AKT and PI3k phosphorylation which indicated APS may exert its function by NRG1/ErbB and the downstream AKT/PI3K signaling. Canertinib is ErbB inhibitor. The effect of APS on proliferation, apoptosis, antioxidation and NRG1/ErbB pathway was partly abolished after the cells were co-treated with APS and canertinib. Taken together, these results suggested APS may display its protective function in DCM cells by activating NGR1/ErbB signaling pathway. And our study increased potential for prevention and therapy to DCM.

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“…While circulating NRG1 has previously been shown to act directly on the central nervous system [22,55] , liver [36,55] , skeletal muscle [56] , and cardiac muscle [24] here we propose an additional site of action within adipose tissues. We present a model that Type III NRG1 is epigenetically regulated and endogenously produced within adipose as a molecular rheostat controlling adipose expandability.…”

Section: Discussionmentioning

confidence: 63%

Epigenetic regulation of Neuregulin-1 tunes white adipose stem cell differentiation

Cordero

Callihan

Said

et al. 2020

Preprint

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AbstractExpansion of subcutaneous adipose tissue by differentiation of new adipocytes has been linked to improvements in metabolic health. However, an expandability limit has been observed wherein new adipocytes cannot be produced, the existing adipocytes become enlarged (hypertrophic) and lipids spill over into ectopic sites. Inappropriate ectopic storage of these surplus lipids in liver, muscle, and visceral depots has been linked with metabolic dysfunction. Here we show that Neuregulin-1 (NRG1) serves as a regulator of adipogenic differentiation in subcutaneous primary human stem cells. We further demonstrate that DNA methylation modulates NRG1 expression in these cells, and a 3-day exposure of stem cells to a recombinant NRG1 peptide fragment is sufficient to reprogram adipogenic cellular differentiation to higher levels. These results define a novel molecular adipogenic rheostat with potential implications for the expansion of adipose tissue in vivo.

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Neuregulin 1 improves complex 2-mediated mitochondrial respiration in skeletal muscle of healthy and diabetic mice

Cited by 20 publications

References 55 publications

Modulation of the Neuregulin 1/ErbB system after skeletal muscle denervation and reinnervation

Modulation of the Neuregulin 1/ErbB system after skeletal muscle denervation and reinnervation

<i>Astraglaus polysaccharide</i> protects diabetic cardiomyopathy by activating NRG1/ErbB pathway

Epigenetic regulation of Neuregulin-1 tunes white adipose stem cell differentiation

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