PGC-1β-Regulated mitochondrial biogenesis and function in myotubes is mediated by NRF-1 and ERRα

Шао, Ди; Liu, Yang; Liu, Xiaojun; Zhu, Linyu; Cui, Ying; Cui, Anfang; Qiao, Aijun; Kong, Xingxing; Liu, Yong; Chen, Quan; Gupta, Nishith; Fang, Fude; Chang, Yongsheng

doi:10.1016/j.mito.2010.05.012

Cited by 129 publications

(111 citation statements)

References 43 publications

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“…For instance, enhancing (29,42,52) or suppressing (23, 55) mitochondrial biogenesis potently alters myogenic differentiation of myoblasts in culture and animal models. The formation of myotube was severely impaired in PGC-1␤ knockdown model or mtDNA-depleted myoblasts (55). Moreover, previous studies showed that defects in mitochondrial fusion and fission processes were asso- ciated with failure of normal mitochondrial proliferation (15).…”

Section: Discussionmentioning

confidence: 94%

Inhibition of Drp1-dependent mitochondrial division impairs myogenic differentiation

Kim

Yoon

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Mitochondria are dynamic organelles forming a tubular network that is continuously fusing and dividing to control their morphology and functions. Recent literature has shed new light on a potential link between the dynamic behavior of mitochondria and muscle development. In this study, we investigate the role of mitochondrial fission factor dynamin-related protein 1 (Drp1) in myogenic differentiation. We found that differentiation of C2C12 myoblasts induced by serum starvation was accompanied by a gradual increase in Drp1 protein expression (to ∼350% up to 3 days) and a fast reduction of Drp1 phosphorylation at Ser-637 (to ∼30%) resulting in translocation of Drp1 protein from the cytosol to mitochondria. During differentiation, treatment of myoblasts with mitochondrial division inhibitor ( mdivi-1), a specific inhibitor of Drp1 GTPase activity, caused extensive formation of elongated mitochondria, which coincided with increased apoptosis evidenced by both enhanced caspase-3 activity and increased number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells. Furthermore, the mdivi-1-treated myotubes ( day 3 in differentiation media) showed a reduction in mitochondrial DNA content, mitochondrial mass, and membrane potential in a dose-dependent manner indicating defects in mitochondrial biogenesis during myogenic differentiation. Most interestingly, mdivi-1 treatment significantly suppressed myotube formation in both C2C12 cells and primary myoblasts. Likewise, stable overexpression of a dominant negative mutant Drp1 (K38A) dramatically reduced myogenic differentiation. These data suggest that Drp-1-dependent mitochondrial division is a necessary step for successful myogenic differentiation, and perturbation of mitochondrial dynamics hinders normal mitochondrial adaptations during muscle development. Therefore, in the present study, we report a novel physiological role of mitochondrial dynamics in myogenic differentiation.

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Section: Discussionmentioning

confidence: 94%

Inhibition of Drp1-dependent mitochondrial division impairs myogenic differentiation

Kim

Yoon

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…These include the sirtuins and 5′ AMP-activated protein kinase pathway, 156 estrogen related receptor (ERR)-α, 157 estrogen related receptor (ERR)-γ, 158 and nuclear respiratory factor 1. 159 Although the use of the 5′ AMP-activated protein kinase activator 5-aminoimidazole-4-carboxamide ribonucleotide for doping in cycling and other professional sports is suspect, clinical trial results assessing its effect on performance have been generally disappointing. 160 However, lack of benefit in healthy subjects may not exclude effectiveness in patients with PAD.…”

Section: Skeletal Muscle Metabolic Abnormalitiesmentioning

confidence: 99%

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Hiatt¹,

Armstrong²,

Larson³

et al. 2015

Circulation Research

137

118

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P eripheral artery disease (PAD) is initiated by atherogenic mechanisms common to all major vascular territories but encompasses several distinctly important clinical sequelae.1 The global burden of PAD is large and rising, with substantial morbidity and mortality found in high-, middle-, and low-income countries. 2 The atherosclerotic occlusive disease underlying PAD is associated with an exercise limitation in the majority of patients, whereas the classic symptoms of intermittent claudication, ischemic rest pain, and ischemic ulceration are less common manifestations. 3 Patients with PAD are also at increased risk of myocardial infarction, ischemic stroke, heart failure, renovascular hypertension, and vascular death reflecting the systemic atherosclerotic burden. [4][5][6] The epidemiology of Peripheral Artery Disease Compendium© 2015 American Heart Association, Inc. The diagnosis of PAD can be ascertained by simple hemodynamic measurements, in particular, the ankle-brachial index (ABI), a test performed by measuring the systolic blood pressure in each arm and the dorsalis pedis and posterior tibial arteries of each ankle. The highest of the dorsalis pedis or posterior tibial artery pressures is the numerator of the ABI specific to each leg, whereas the highest arm pressure on either side is the denominator. A ratio of <0.90 in either leg is considered hemodynamic evidence of PAD. 16 When imaged, PAD can be characterized as one or more arterial stenoses or occlusions involving the distal aorta, iliac, femoral, popliteal, or tibial arteries. 17The underlying mechanisms responsible for the functional limitations in PAD are hemodynamic in origin, which affects the supply of oxygen and substrates to metabolically active tissue: skeletal muscle in the case of intermittent claudication and skin and subcutaneous tissues in the case of critical leg ischemia. However, additional pathophysiologic mechanisms contribute to the limb manifestations, where a reduction in blood flow alone does not fully account for the exercise limitation. Recent research into the pathophysiology of this exercise limitation has identified several important sequelae resultant from the chronic hemodynamic deficit. These changes affecting the vasculature and skeletal muscle distal to the primary hemodynamic lesions likely contribute to the mechanisms of exercise limitation in PAD. These advances are reviewed here with an additional focus on identifying possible future therapeutic strategies. Symptomatic Manifestations and Exercise Limitations in PADIn the coronary circulation, plaque rupture leading to acute ischemic events is a common clinical presentation; in PAD, progressive atherosclerosis leading to chronic stenosis and occlusion, often in series, in the arteries supplying the lower extremities dominates the symptomatic manifestations.6 Limb SymptomsPatients with PAD may present with a range of limb symptoms. Most patients are either asymptomatic or have atypical limb symptoms during exercise, whereas only a third have typical symptoms of c...

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“…The peroxisome proliferator-activated receptor (PPAR)-␥ coactivator 1 (PGC-1) family of transcriptional coactivator molecules plays a key role in the regulation of mitochondrial biogenesis and determination of muscle OXPHEN as they interact with and coactivate numerous DNA-binding transcription factors to control the regulation of multiple genes encoding mitochondrial proteins. Transcription factors coactivated by PGC-1 include PPAR-␣ and PPAR-␦, estrogen-related receptor ␣ (ERR-␣), nuclear respiratory factor (NRF) 1, and NRF-2␣ (21,38). Whereas PPAR molecules are involved in the transcription of genes coding for proteins involved in fatty acid uptake, transport, and oxidation (20), NRF-1 and NRF-2␣ transcribe constituents of the mitochondrial oxidative phosphorylation (OXPHOS) chain itself (2).…”

mentioning

confidence: 99%

Activation of alternative NF-κB signaling during recovery of disuse-induced loss of muscle oxidative phenotype

Remels

Pansters

Gosker

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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PGC-1β-Regulated mitochondrial biogenesis and function in myotubes is mediated by NRF-1 and ERRα

Cited by 129 publications

References 43 publications

Inhibition of Drp1-dependent mitochondrial division impairs myogenic differentiation

Inhibition of Drp1-dependent mitochondrial division impairs myogenic differentiation

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Activation of alternative NF-κB signaling during recovery of disuse-induced loss of muscle oxidative phenotype

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