CD34 regulates the skeletal muscle response to hypoxia

Page, Melissa M.; Maheux, Catherine; Langlois, Anick; Brassard, Julyanne; Bernatchez, Emilie; Martineau, Sandra; Henry, Cyndi; Beaulieu, Marie‐Josée; Bossé, Ynuk; Morissette, Mathieu C.; Debigaré, Richard; Blanchet, Marie‐Renée

doi:10.1007/s10974-019-09525-x

Cited by 3 publications

(6 citation statements)

References 46 publications

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“…In experimental models, hypoxia clearly induces muscle wasting, as evidenced by several reports showing muscle atrophy even after only few days of hypoxia exposure [ 67 , 68 ]. At the structural level, hypoxia might favor a fiber-type switch in the muscle of COPD patients [ 69 ].…”

Section: Hypoxia and Hypercapniamentioning

confidence: 99%

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Henrot

Dupin

Schilfarth

et al. 2023

IJMS

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Chronic obstructive pulmonary disease (COPD) is a worldwide prevalent respiratory disease mainly caused by tobacco smoke exposure. COPD is now considered as a systemic disease with several comorbidities. Among them, skeletal muscle dysfunction affects around 20% of COPD patients and is associated with higher morbidity and mortality. Although the histological alterations are well characterized, including myofiber atrophy, a decreased proportion of slow-twitch myofibers, and a decreased capillarization and oxidative phosphorylation capacity, the molecular basis for muscle atrophy is complex and remains partly unknown. Major difficulties lie in patient heterogeneity, accessing patients’ samples, and complex multifactorial process including extrinsic mechanisms, such as tobacco smoke or disuse, and intrinsic mechanisms, such as oxidative stress, hypoxia, or systemic inflammation. Muscle wasting is also a highly dynamic process whose investigation is hampered by the differential protein regulation according to the stage of atrophy. In this review, we report and discuss recent data regarding the molecular alterations in COPD leading to impaired muscle mass, including inflammation, hypoxia and hypercapnia, mitochondrial dysfunction, diverse metabolic changes such as oxidative and nitrosative stress and genetic and epigenetic modifications, all leading to an impaired anabolic/catabolic balance in the myocyte. We recapitulate data concerning skeletal muscle dysfunction obtained in the different rodent models of COPD. Finally, we propose several pathways that should be investigated in COPD skeletal muscle dysfunction in the future.

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Section: Hypoxia and Hypercapniamentioning

confidence: 99%

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Henrot

Dupin

Schilfarth

et al. 2023

IJMS

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“…Previous studies have demonstrated pathological hypoxia-induced skeletal muscle myoblast injury, including the inhibition of viability and differentiation (43)(44)(45). Regarding viability, cocl 2 produced changes typical of cell death, such as characteristic cell extension, increased volume, chromatin condensation and G2/M phase cell cycle arrest, ultimately leading to reduced proliferation (13).…”

Section: Discussionmentioning

confidence: 98%

The secretome of human dental pulp stem cells protects myoblasts from hypoxia‑induced injury via the Wnt/β‑catenin pathway

Zhang

Han

et al. 2020

Int J Mol Med

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Human dental pulp stem cells (hdPScs) present several advantages, including their ability to be non-invasively harvested without ethical concern. The secretome of hdPScs can promote the functional recovery of various tissue injuries. However, the protective effects on hypoxia-induced skeletal muscle injury remain to be explored. The present study demonstrated that c2c12 myoblast coculture with hdPScs attenuated cocl 2-induced hypoxic injury compared with c2c12 alone. The hdPSc secretome increased cell viability and differentiation and decreased G2/M cell cycle arrest under hypoxic conditions. These results were further verified using hDPSC-conditioned medium (hDPSC-CM). The present data revealed that the protective effects of hdPSc-cM depend on the concentration ratio of the cM. In terms of the underlying molecular mechanism, hdPSc-cM activated the Wnt/β-catenin pathway, which increased the protein levels of Wnt1, phosphorylated-glycogen synthase kinase-3β and β-catenin and the mRNA levels of Wnt target genes. By contrast, an inhibitor (XAV939) of Wnt/β-catenin diminished the protective effects of hdPSc-cM. Taken together, the findings of the present study demonstrated that the hDPSC secretome alleviated the hypoxia-induced myoblast injury potentially through regulating the Wnt/β-catenin pathway. These findings may provide new insight into a therapeutic alternative using the hdPSc secretome in skeletal muscle hypoxia-related diseases.

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“…44 Moreover, CD34 À/À mice suffer from more severe muscle atrophy induced by hypoxia than wild-type mice, and this seems to be at least partly mediated by a lower number of FAPs. 45 Overall, the role of FAPs in skeletal muscle tissue has mainly been characterized in regeneration, where they take part in both phases by secreting growth factors and cytokines. In other diseases, they are mainly associated with muscle fibrosis, for example, in models of chronic kidney disease, upon stimulation by myostatin.…”

Section: Progenitor Cellsmentioning

confidence: 99%

“…This physiological response is disrupted in the case of chronic trauma or disease such as Duchenne muscular dystrophy, where FAPs are responsible for prolonged connective tissue production and muscle fibrosis 44 . Moreover, CD34 −/− mice suffer from more severe muscle atrophy induced by hypoxia than wild‐type mice, and this seems to be at least partly mediated by a lower number of FAPs 45 …”

Section: Introductionmentioning

confidence: 99%

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Cellular interplay in skeletal muscle regeneration and wasting: insights from animal models

Henrot

Blervaque

Dupin

et al. 2023

J cachexia sarcopenia muscle

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Skeletal muscle wasting, whether related to physiological ageing, muscle disuse or to an underlying chronic disease, is a key determinant to quality of life and mortality. However, cellular basis responsible for increased catabolism in myocytes often remains unclear. Although myocytes represent the vast majority of skeletal muscle cellular population, they are surrounded by numerous cells with various functions. Animal models, mostly rodents, can help to decipher the mechanisms behind this highly dynamic process, by allowing access to every muscle as well as time-course studies. Satellite cells (SCs) play a crucial role in muscle regeneration, within a niche also composed of fibroblasts and vascular and immune cells. Their proliferation and differentiation is altered in several models of muscle wasting such as cancer, chronic kidney disease or chronic obstructive pulmonary disease (COPD). Fibro-adipogenic progenitor cells are also responsible for functional muscle growth and repair and are associated in disease to muscle fibrosis such as in chronic kidney disease. Other cells have recently proven to have direct myogenic potential, such as pericytes. Outside their role in angiogenesis, endothelial cells and pericytes also participate to healthy muscle homoeostasis by promoting SC pool maintenance (so-called myogenesis-angiogenesis coupling). Their role in chronic diseases muscle wasting has been less studied. Immune cells are pivotal for muscle repair after injury: Macrophages undergo a transition from the M1 to the M2 state along with the transition between the inflammatory and resolutive phase of muscle repair. T regulatory lymphocytes promote and regulate this transition and are also able to activate SC proliferation and differentiation. Neural cells such as terminal Schwann cells, motor neurons and kranocytes are notably implicated in age-related sarcopenia. Last, newly identified cells in skeletal muscle, such as telocytes or interstitial tenocytes could play a role in tissular homoeostasis. We also put a special focus on cellular alterations occurring in COPD, a chronic and highly prevalent respiratory disease mainly linked to tobacco smoke exposure, where muscle wasting is strongly associated with increased mortality, and discuss the pros and cons of animal models versus human studies in this context. Finally, we discuss resident cells metabolism and present future promising leads for research, including the use of muscle organoids.

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CD34 regulates the skeletal muscle response to hypoxia

Cited by 3 publications

References 46 publications

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

The secretome of human dental pulp stem cells protects myoblasts from hypoxia‑induced injury via the Wnt/β‑catenin pathway

Cellular interplay in skeletal muscle regeneration and wasting: insights from animal models

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