Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Oyaizu, Takuya; Enomoto, Mitsuhiro; Yamamoto, Naoki; Tsuji, Kunikazu; Horie, Masaki; Muneta, Takeshi; Sekiya, Ichiro; Okawa, Atsushi; Yagishita, Kazuyoshi

doi:10.1038/s41598-018-19670-x

Cited by 67 publications

(51 citation statements)

References 41 publications

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“…The gene set of "negative regulation of immune response" was enriched in HBO group suggesting an inflammation inhibition effect too. The immune inhibition information we get from the DEG analysis and GSEA are consistent with the reduction in lipofibroblasts, which characteristically show activation of inflammation, and consistent with the reports that HBO exposure attenuate inflammation in a few of conditions [56][57][58][59][60][61].…”

Section: Discussionsupporting

confidence: 89%

Deconvolution of RNA-Seq Analysis of Hyperbaric Oxygen-Treated Mice Lungs Reveals Mesenchymal Cell Subtype Changes

Yuan

Zhou

et al. 2020

IJMS

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Hyperbaric oxygen (HBO) is widely applied to treat several hypoxia-related diseases. Previous studies have focused on the immediate effect of HBO-exposure induced oxidative stress on the lungs, but knowledge regarding the chronic effects from repetitive HBO exposure is limited, especially at the gene expression level. We found that repetitive HBO exposure did not alter the morphology of murine lungs. However, by deconvolution of RNA-seq from those mice lungs using CIBERSORTx and the expression profile matrices of 8 mesenchymal cell subtypes obtained from bleomycin-treated mouse lungs, we identify several mesenchymal cell subtype changes. These include increases in Col13a1 matrix fibroblasts, mesenchymal progenitors and mesothelial cell populations and decreases in lipofibroblasts, endothelial and Pdgfrb high cell populations. Our data suggest that repetitive HBO exposure may affect biological processes in the lungs such as response to wounding, extracellular matrix, vasculature development and immune response.

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Section: Discussionsupporting

confidence: 89%

Deconvolution of RNA-Seq Analysis of Hyperbaric Oxygen-Treated Mice Lungs Reveals Mesenchymal Cell Subtype Changes

Yuan

Zhou

et al. 2020

IJMS

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“…Subsequently, the laminin is re-formed, and the abnormal proliferation of blood vessel cells ceases. The blood vessels then become mature, and angiogenesis is completed at 7 to 14 days 13,32 . In the HBO group in the present study, the number of proliferating endothelial cells was increased at 1 day after injury, and then the number of immature vessels increased at 3 days and decreased from 5 days after injury.…”

Section: Discussionmentioning

confidence: 99%

“…HBO has been reported as an additional treatment for skeletal muscle injury, as HBO is clinically considered to promote muscle regeneration 28,29 and accelerate the return to competition 30 . Our previous study showed that HBO accelerated the recovery of intact muscle volume, stimulated satellite cell proliferation, and promoted muscle regeneration via macrophage recruitment 31,32 . In a previous study, HBO increased mRNA levels of bFGF and HGF without upregulation of VEGF, increasing and promoted angiogenesis and muscle regeneration after ischemic muscle injury 6 .…”

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confidence: 99%

VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration

Yamamoto

Oyaizu

Enomoto

et al. 2020

Sci Rep

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Hyperbaric oxygen (HBo) treatment promotes early recovery from muscle injury. Reactive oxygen species (ROS) upregulation is a key mechanism of HBO, which produces high O 2 content in tissues through increased dissolution of oxygen at high pressure. Nitric oxide (NO), a type of ROS, generally stabilizes hypoxia-inducible factor (HIF) 1α and stimulates secretion of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) from endothelial cells and macrophages, which then induces angiogenesis. the purpose of the present study was to investigate whether HBo could promote angiogenesis via induction of no and induce muscle regeneration in contused rat skeletal muscles. The HBO protocol consisted of 2.5 atmospheres absolute (ATA) 100% oxygen for 120 minutes, once a day for 5 consecutive days. We also evaluated the effects of a ROS inhibitor (NAC) or NOS-specific inhibitor (L-NAME) on HBO. HBO significantly increased NO 3 − , VEGF, and bFGF levels and stabilized HIF1α within 1 day. HBO promoted blood vessel formation at 3-7 days and muscle healing at 5-7 days after contusion. Administration of both NAC and L-NAME before HBO suppressed angiogenesis and muscle regeneration even after HBo. HBo thus promoted angiogenesis and muscle regeneration mainly through generation of no in the early phase after muscle contusion injury. Muscle contusion injury is one of the common injuries in sports medicine 1. Among muscle injuries, 90% are caused by contusions 2 produced by high-energy blunt trauma from a non-penetrating object, or by excessive strain of the muscle 3. Such injuries are usually treated non-operatively following the RICE (rest, ice, compression, and elevation) protocol and a short period of immobilization, followed by active and passive range-of-motion exercises 3. In severe cases, muscle contusions cause vascular disruption 4,5. Acute ischemia induces gradual deterioration of energy metabolism in muscle, followed by cell death or adaptation 6. Delayed vascular repair can delay muscle regeneration, which may lead to increased fibrosis in skeletal muscle. It has been reported that decreased blood supply caused by delayed vascular repair delays the regeneration of soft tissue 7. Thus, muscle regeneration, collateral formation, and angiogenesis are likely related, and blood vessel formation after injury is also essential for muscle regeneration 2,8. Early and efficient recovery of blood vessels may be important for recovery of motor function, especially with regard to muscle tensile strength, and may enable an early return to sports for athletes. Thus, early and appropriate treatment strategies for severe muscle injury focusing on angiogenesis are required. After injury, among the factors associated angiogenesis, upregulation of VEGF 9-11 , basic fibroblast growth factor (bFGF) 6,11 , hepatocyte growth factor (HGF) 6 , and angiopoietin 2 11 activates migration and proliferation of endothelial cells, and promotes angiogenesis 12,13 Moreover, it has been reported that stabilization of hypoxia-induc...

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“…According to the team of Yagishita, STAT3 phosphorylation is a major step in satellite cell activation and tissue repair. Whether in diabetic patients, the progenitor cell activation contributes toward wound healing and conservation of cardiovascular status, needs to be further assessed [35].…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Therapy Dampens Inflammatory Cytokine Production and Does Not Worsen the Cardiac Function and Oxidative State of Diabetic Rats

et al. 2019

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Hyperbaric oxygen therapy (HBOT) is frequently used after soft tissue injuries and in diabetic patients with ulcerated wounds; however, its ability to increase oxidative stress casts doubts. Diabetes (DM) in male Wistar rats (N = 20) weighing 300 g were induced by a single dose of streptozotocin. Ten diabetics (DMHBOT) and 10 controls (CHBOT) underwent a one-hour long hyperbaric oxygen treatment protocol (2.5 bar) 12 times after the 3rd week of diabetes. Ten animals remained untreated. Eight weeks after diabetes induction, we measured the 24-hour blood glucose profile and cardiovascular function (sonocardiography and the relaxation ability of aortae). Malonyl-dialdehyde (MDA) and cytokine levels were measured in blood plasma. Poly(ADP-ribose) polymerase (PARP) activity was estimated in cardiac and aortic tissue. HBOT did not alter most of the cardiovascular parameters. PARylation in cardiac and aortic tissues, plasma MDA levels were elevated in diabetic rats. HBOT prevented the increase of MDA in diabetic animals. In addition, levels of the pro-inflammatory cytokine-induced neutrophil chemoattractant-1 (CINC-1) the levels of anti-inflammatory tissue inhibitor of metalloproteases-1 were not altered in diabetes or in hyperoxia. Our results suggest that HBOT does not increase long-term oxidative stress, and, similar to training, the TBARS products, nitrotyrosine formation and poly(ADP-ribosyl)ation may be eased as a result of hyperoxia.

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Hyperbaric oxygen reduces inflammation, oxygenates injured muscle, and regenerates skeletal muscle via macrophage and satellite cell activation

Cited by 67 publications

References 41 publications

Deconvolution of RNA-Seq Analysis of Hyperbaric Oxygen-Treated Mice Lungs Reveals Mesenchymal Cell Subtype Changes

Deconvolution of RNA-Seq Analysis of Hyperbaric Oxygen-Treated Mice Lungs Reveals Mesenchymal Cell Subtype Changes

VEGF and bFGF induction by nitric oxide is associated with hyperbaric oxygen-induced angiogenesis and muscle regeneration

Hyperbaric Oxygen Therapy Dampens Inflammatory Cytokine Production and Does Not Worsen the Cardiac Function and Oxidative State of Diabetic Rats

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